https://www.wikidoc.org/api.php?action=feedcontributions&feedformat=atom&user=Jogeet+singh+sekhon 2026-04-13T03:42:19Z User contributions MediaWiki 1.45.1 https://www.wikidoc.org/index.php?title=Lipoma_screening&diff=1556941 2019-03-07T14:23:37Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> {{PleaseHelp}}<br /> <br /> ==Overview==<br /> Screening for lipoma is not recommended.<br /> <br /> ==Screening==<br /> * Screening for lipoma is not done.<br /> * Lipomas are usually discovered as an incidental finding or when patient reports with symptoms.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Needs overview]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_epidemiology_and_demographics&diff=1556940 2019-03-07T14:22:32Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> {{PleaseHelp}}<br /> ==Overview==<br /> Lipoma is a common disease. Patients of all age groups may develop it, however its more common occur in middle age, especially people from 40-60 years old.<br /> ==Epidemiology and Demographics==<br /> ===Incidence===<br /> * Approximately one percent of the general population has a lipoma.&lt;ref name=&quot;emedicine2720&quot;&gt;{{EMedicine|med|2720|Lipomas}}&lt;/ref&gt; <br /> ===Age===<br /> * These tumors can occur at any age, but are most common in middle age, often appearing in people from 40 to 60 years old.&lt;ref name=&quot;Salam&quot;&gt;{{cite journal |author=Salam GA |title=Lipoma excision |journal=Am Fam Physician |volume=65 |issue=5 |pages=901–4 |date=March 2002 |pmid=11898962 |url=http://www.aafp.org/afp/20020301/901.html}}&lt;/ref&gt; <br /> * Cutaneous lipomas are rare in children, but these tumors can occur as part of the inherited disease [[Bannayan-Zonana syndrome]].&lt;ref&gt;{{cite journal |author=Buisson P, Leclair MD, Jacquemont S, ''et al.'' |title=Cutaneous lipoma in children: 5 cases with Bannayan-Riley-Ruvalcaba syndrome |journal=J. Pediatr. Surg. |volume=41 |issue=9 |pages=1601–3 |date=September 2006 |pmid=16952599 |doi=10.1016/j.jpedsurg.2006.05.013}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Gujrati M, Thomas C, Zelby A, Jensen E, Lee JM |title=Bannayan-Zonana syndrome: a rare autosomal dominant syndrome with multiple lipomas and hemangiomas: a case report and review of literature |journal=Surg Neurol |volume=50 |issue=2 |pages=164–8 |date=August 1998 |pmid=9701122 |doi= 10.1016/S0090-3019(98)00039-1|url=http://linkinghub.elsevier.com/retrieve/pii/S0090-3019(98)00039-1}}&lt;/ref&gt;<br /> <br /> === Gender ===<br /> * There is no difference in occurence of lipoma in men and women.<br /> <br /> === Race ===<br /> * Lipoma develops in all races equally.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_causes&diff=1556939 2019-03-07T14:19:40Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}} <br /> <br /> ==Overview==<br /> Lipoma may be caused by either genetic factors, or injury.<br /> <br /> ==Causes==<br /> * '''Heredity'''<br /> ** Conditions, such as [[lipomatosis|familial multiple lipomatosis]], may include lipoma development.&lt;ref&gt;{{cite journal |author=Leffell DJ, Braverman IM |title=Familial multiple lipomatosis. Report of a case and a review of the literature |journal=J. Am. Acad. Dermatol. |volume=15 |issue=2 Pt 1 |pages=275–9 |date=August 1986 |pmid=3745530 |doi=10.1016/S0190-9622(86)70166-7}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Toy BR |title=Familial multiple lipomatosis |journal=Dermatol. Online J. |volume=9 |issue=4 |pages=9 |date=October 2003 |pmid=14594582 |url=http://dermatology.cdlib.org/94/NYU/Jan2002/2.html}}&lt;/ref&gt; <br /> ** Genetic studies have shown a correlation between the ''HMG I-C'' gene and lipoma development.<br /> <br /> * '''Trauma'''<br /> :Minor injuries are alleged to have triggered the growth of a lipoma, called &quot;post-traumatic lipomas&quot;&lt;ref&gt;{{cite journal |author=Signorini M, Campiglio GL |title=Posttraumatic lipomas: where do they really come from? |journal=Plast. Reconstr. Surg. |volume=101 |issue=3 |pages=699–705 |date=March 1998 |pmid=9500386 |doi=10.1097/00006534-199803000-00017}}&lt;/ref&gt;.&lt;ref&gt;{{cite journal |author=Aust MC, Spies M, Kall S, Jokuszies A, Gohritz A, Vogt P |title=Posttraumatic lipoma: fact or fiction? |journal=Skinmed |volume=6 |issue=6 |pages=266–70 |year=2007 |pmid=17975353 |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_6;6:266 |doi=10.1111/j.1540-9740.2007.06361.x}}&lt;/ref&gt;<br /> :Trauma-induced [[cytokine]] release triggers pre-adipocyte differentiation and maturation which leads to the formation of pseudolipomas that progress to lipomas.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_natural_history,_complications_and_prognosis&diff=1556448 2019-03-05T20:57:08Z

<p>Jogeet singh sekhon: /* Natural History */</p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> ==Overview==<br /> Common complications of lipoma include [[bleeding]], [[ulceration]], malignant transformation, and recurrence. Prognosis is generally excellent. <br /> <br /> ==Natural History==<br /> <br /> ==Complications==<br /> The complications of lipoma listed below:<br /> * [[Bleeding]]<br /> * [[Ulceration]]<br /> * [[Malignant]] transformation<br /> * Recurrence<br /> <br /> ==Prognosis==<br /> * Lipomas are rarely life-threatening and the common subcutaneous lipomas are not a serious condition. Lipomas growing in internal organs can be more dangerous. &lt;ref&gt;{{cite journal |author=Thompson WM |title=Imaging and findings of lipomas of the gastrointestinal tract |journal=AJR Am J Roentgenol |volume=184 |issue=4 |pages=1163–71 |date=1 April 2005|pmid=15788588 |url=http://www.ajronline.org/cgi/pmidlookup?view=long&amp;pmid=15788588 |doi=10.2214/ajr.184.4.01841163}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Taylor AJ, Stewart ET, Dodds WJ |title=Gastrointestinal lipomas: a radiologic and pathologic review |journal=AJR Am J Roentgenol |volume=155 |issue=6 |pages=1205–10 |date=1 December 1990|pmid=2122666 |url=http://www.ajronline.org/cgi/pmidlookup?view=long&amp;pmid=2122666 |doi=10.2214/ajr.155.6.2122666}}&lt;/ref&gt; <br /> * Malignant transformation of lipomas into [[liposarcoma]]s is very rare and most liposarcomas are not produced from pre-existing benign lesions. A few cases of malignant transformation have been described for bone and kidney lipomas,&lt;ref&gt;{{cite journal |author=Milgram JW |title=Malignant transformation in bone lipomas |journal=Skeletal Radiol. |volume=19 |issue=5 |pages=347–52 |year=1990 |pmid=2165632 |doi=10.1007/BF00193088}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Lowe BA, Brewer J, Houghton DC, Jacobson E, Pitre T |title=Malignant transformation of angiomyolipoma |journal=J. Urol. |volume=147 |issue=5 |pages=1356–8 |date=May 1992 |pmid=1569683}}&lt;/ref&gt; but it is possible these few reported cases were well-differentiated liposarcomas in which the subtle [[malignant]] characteristics were missed when the tumour was first examined.&lt;ref name=&quot;Enzinger08&quot;&gt;{{cite book |author=Goldblum, John R.; Weiss, Sharon W.; Enzinger, Franz M. |title=Enzinger and Weiss's soft tissue tumors |publisher=Mosby Elsevier |year=2008 |isbn=0-323-04628-2 |edition=5th}}&lt;/ref&gt; <br /> * Deep lipomas have a greater tendency to recur than superficial lipomas, because complete surgical removal of deep lipomas is not always possible.&lt;ref&gt;{{cite book |author=Fletcher, C.D.M., Unni, K.K., Mertens, F. |title=Pathology and Genetics of Tumours of Soft Tissue and Bone |publisher=IARC Press |location=Lyon |year=2002 |isbn=92-832-2413-2 |series=World Health Organization Classification of Tumours |volume=4}}&lt;/ref&gt;<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_screening&diff=1556393 2019-03-05T19:57:24Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> {{PleaseHelp}}<br /> <br /> ==Overview==<br /> Screening for lipoma is not recommended.<br /> <br /> ==Screening==<br /> * Screening for lipoma is not done.<br /> * Lipomas are usually discovered as an incidental finding.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Needs overview]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_causes&diff=1556392 2019-03-05T19:54:17Z

<p>Jogeet singh sekhon: /* Causes */</p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}} <br /> <br /> ==Overview==<br /> Lipoma may be caused by either genetic factors, or injury.<br /> <br /> ==Causes==<br /> * '''Heredity'''<br /> ** Conditions, such as [[lipomatosis|familial multiple lipomatosis]], may include lipoma development.&lt;ref&gt;{{cite journal |author=Leffell DJ, Braverman IM |title=Familial multiple lipomatosis. Report of a case and a review of the literature |journal=J. Am. Acad. Dermatol. |volume=15 |issue=2 Pt 1 |pages=275–9 |date=August 1986 |pmid=3745530 |doi=10.1016/S0190-9622(86)70166-7}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Toy BR |title=Familial multiple lipomatosis |journal=Dermatol. Online J. |volume=9 |issue=4 |pages=9 |date=October 2003 |pmid=14594582 |url=http://dermatology.cdlib.org/94/NYU/Jan2002/2.html}}&lt;/ref&gt; <br /> ** Genetic studies have shown a correlation between the ''HMG I-C'' gene and lipoma development.<br /> <br /> * '''Trauma'''<br /> :Minor injuries are alleged to have triggered the growth of a lipoma, called &quot;post-traumatic lipomas&quot;&lt;ref&gt;{{cite journal |author=Signorini M, Campiglio GL |title=Posttraumatic lipomas: where do they really come from? |journal=Plast. Reconstr. Surg. |volume=101 |issue=3 |pages=699–705 |date=March 1998 |pmid=9500386 |doi=10.1097/00006534-199803000-00017}}&lt;/ref&gt;.&lt;ref&gt;{{cite journal |author=Aust MC, Spies M, Kall S, Jokuszies A, Gohritz A, Vogt P |title=Posttraumatic lipoma: fact or fiction? |journal=Skinmed |volume=6 |issue=6 |pages=266–70 |year=2007 |pmid=17975353 |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_6;6:266 |doi=10.1111/j.1540-9740.2007.06361.x}}&lt;/ref&gt;<br /> :Trauma-induced cytokine release triggers pre-adipocyte differentiation and maturation which leads to the formation of pseudolipomas that progress to lipomas.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_causes&diff=1556391 2019-03-05T19:51:51Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}} <br /> <br /> ==Overview==<br /> Lipoma may be caused by either genetic factors, or injury.<br /> <br /> ==Causes==<br /> * '''Heredity'''<br /> ** Conditions, such as [[lipomatosis|familial multiple lipomatosis]], may include lipoma development.&lt;ref&gt;{{cite journal |author=Leffell DJ, Braverman IM |title=Familial multiple lipomatosis. Report of a case and a review of the literature |journal=J. Am. Acad. Dermatol. |volume=15 |issue=2 Pt 1 |pages=275–9 |date=August 1986 |pmid=3745530 |doi=10.1016/S0190-9622(86)70166-7}}&lt;/ref&gt;&lt;ref&gt;{{cite journal |author=Toy BR |title=Familial multiple lipomatosis |journal=Dermatol. Online J. |volume=9 |issue=4 |pages=9 |date=October 2003 |pmid=14594582 |url=http://dermatology.cdlib.org/94/NYU/Jan2002/2.html}}&lt;/ref&gt; <br /> ** Genetic studies have shown a correlation between the ''HMG I-C'' gene and lipoma development.<br /> <br /> * '''Trauma'''<br /> :Minor injuries are alleged to have triggered the growth of a lipoma, called &quot;post-traumatic lipomas&quot;&lt;ref&gt;{{cite journal |author=Signorini M, Campiglio GL |title=Posttraumatic lipomas: where do they really come from? |journal=Plast. Reconstr. Surg. |volume=101 |issue=3 |pages=699–705 |date=March 1998 |pmid=9500386 |doi=10.1097/00006534-199803000-00017}}&lt;/ref&gt;.&lt;ref&gt;{{cite journal |author=Aust MC, Spies M, Kall S, Jokuszies A, Gohritz A, Vogt P |title=Posttraumatic lipoma: fact or fiction? |journal=Skinmed |volume=6 |issue=6 |pages=266–70 |year=2007 |pmid=17975353 |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_6;6:266 |doi=10.1111/j.1540-9740.2007.06361.x}}&lt;/ref&gt;<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_historical_perspective&diff=1556390 2019-03-05T19:48:53Z

<p>Jogeet singh sekhon: /* Historical Perspective */</p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> {{PleaseHelp}}<br /> <br /> ==Overview==<br /> Lipoma was first described by Kindblom in 1974.<br /> <br /> ==Historical Perspective==<br /> Lipoma was first described by Kindblom in 1974.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Needs overview]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556387 2019-03-05T19:37:27Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoma can occur as a response to trauma or they can appear sporadically.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3&lt;ref name=&quot;pmid18551755&quot;&gt;{{cite journal| author=Ida CM, Wang X, Erickson-Johnson MR, Wenger DE, Blute ML, Nascimento AG et al.| title=Primary retroperitoneal lipoma: a soft tissue pathology heresy?: report of a case with classic histologic, cytogenetics, and molecular genetic features. | journal=Am J Surg Pathol | year= 2008 | volume= 32 | issue= 6 | pages= 951-4 | pmid=18551755 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=18551755 }} &lt;/ref&gt;.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> === Gross pathology ===<br /> Lipoma is seen as a well circumscribed yellow mass.<br /> <br /> [[File:Angiomyolipoma-7.JPG|thumb|none|200px|Angiomyolipoma Gross Pathology&lt;ref&gt;Image courtesy of Dr Andrew Ryan. [http://www.radiopaedia.org Radiopaedia] (original file [http://radiopaedia.org/cases/angiomyolipoma-7]).[http://radiopaedia.org/licence Creative Commons BY-SA-NC&lt;/ref&gt;]]<br /> <br /> === Microscopic pathology ===<br /> &lt;gallery&gt;<br /> Image:Renal angiomyolipoma (1).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name= aaa&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> Image:Renal angiomyolipoma (2).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name= aaa&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> Image:Renal angiomyolipoma (3).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name= aaa&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> <br /> Image:Renal angiomyolipoma (4) HMB-45 immunostain.JPG|Histopathologic image of renal angiomyolipoma. Nephrectomy specimen. HMB-45 immunostain.&lt;ref name= aaa&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> &lt;/gallery&gt;<br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556386 2019-03-05T19:35:40Z

<p>Jogeet singh sekhon: /* Gross pathology */</p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoma can occur as a response to trauma or they can appear sporadically.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3&lt;ref name=&quot;pmid18551755&quot;&gt;{{cite journal| author=Ida CM, Wang X, Erickson-Johnson MR, Wenger DE, Blute ML, Nascimento AG et al.| title=Primary retroperitoneal lipoma: a soft tissue pathology heresy?: report of a case with classic histologic, cytogenetics, and molecular genetic features. | journal=Am J Surg Pathol | year= 2008 | volume= 32 | issue= 6 | pages= 951-4 | pmid=18551755 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=18551755 }} &lt;/ref&gt;.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> === Gross pathology ===<br /> Lipoma is seen as a well circumscribed yellow mass.<br /> <br /> [[File:Angiomyolipoma-7.JPG|thumb|none|200px|Angiomyolipoma Gross Pathology&lt;ref&gt;Image courtesy of Dr Andrew Ryan. [http://www.radiopaedia.org Radiopaedia] (original file [http://radiopaedia.org/cases/angiomyolipoma-7]).[http://radiopaedia.org/licence Creative Commons BY-SA-NC&lt;/ref&gt;]]<br /> <br /> === Microscopic pathology ===<br /> &lt;gallery&gt;<br /> Image:Renal angiomyolipoma (1).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name=&quot;aaa&quot;&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556384 2019-03-05T19:29:43Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoma can occur as a response to trauma or they can appear sporadically.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3&lt;ref name=&quot;pmid18551755&quot;&gt;{{cite journal| author=Ida CM, Wang X, Erickson-Johnson MR, Wenger DE, Blute ML, Nascimento AG et al.| title=Primary retroperitoneal lipoma: a soft tissue pathology heresy?: report of a case with classic histologic, cytogenetics, and molecular genetic features. | journal=Am J Surg Pathol | year= 2008 | volume= 32 | issue= 6 | pages= 951-4 | pmid=18551755 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=18551755 }} &lt;/ref&gt;.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> === Gross pathology ===<br /> Lipoma is composed of subcuatneous fat including lipoblasts.<br /> <br /> [[File:Angiomyolipoma-7.JPG|thumb|none|200px|Angiomyolipoma Gross Pathology&lt;ref&gt;Image courtesy of Dr Andrew Ryan. [http://www.radiopaedia.org Radiopaedia] (original file [http://radiopaedia.org/cases/angiomyolipoma-7]).[http://radiopaedia.org/licence Creative Commons BY-SA-NC&lt;/ref&gt;]]<br /> <br /> === Microscopic pathology ===<br /> <br /> Image:Renal angiomyolipoma (1).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name=&quot;aaa&quot;&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556383 2019-03-05T19:27:42Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoma can occur as a response to trauma or they can appear sporadically.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3&lt;ref name=&quot;pmid18551755&quot;&gt;{{cite journal| author=Ida CM, Wang X, Erickson-Johnson MR, Wenger DE, Blute ML, Nascimento AG et al.| title=Primary retroperitoneal lipoma: a soft tissue pathology heresy?: report of a case with classic histologic, cytogenetics, and molecular genetic features. | journal=Am J Surg Pathol | year= 2008 | volume= 32 | issue= 6 | pages= 951-4 | pmid=18551755 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=18551755 }} &lt;/ref&gt;.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> === Gross pathology ===<br /> [[File:Angiomyolipoma-7.JPG|thumb|none|200px|Angiomyolipoma Gross Pathology&lt;ref&gt;Image courtesy of Dr Andrew Ryan. [http://www.radiopaedia.org Radiopaedia] (original file [http://radiopaedia.org/cases/angiomyolipoma-7]).[http://radiopaedia.org/licence Creative Commons BY-SA-NC&lt;/ref&gt;]]<br /> <br /> <br /> Image:Renal angiomyolipoma (1).jpg|Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H &amp; E stain.&lt;ref name= aaa&gt;http://librepathology.org/wiki/index.php/Angiomyolipoma&lt;/ref&gt;<br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_CT&diff=1556370 2019-03-05T19:09:18Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> ==Overview==<br /> CT scan is needed if there is suspicion of [[liposarcoma]].<br /> <br /> ==Key CT Findings for Lipoma==<br /> * CT scan is useful in diagnosing intestinal lipomas<br /> * On CT, lipoma is seen as a well delineated mass with absorption density characteristic of fatty tissue.<br /> * Intussuscepted lipoma can also be seen.<br /> * CT scan can also differentiate lipoma from liposarcoma.<br /> <br /> ==Examples of CT Findings for Lipoma==<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556366 2019-03-05T19:06:10Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3&lt;ref name=&quot;pmid18551755&quot;&gt;{{cite journal| author=Ida CM, Wang X, Erickson-Johnson MR, Wenger DE, Blute ML, Nascimento AG et al.| title=Primary retroperitoneal lipoma: a soft tissue pathology heresy?: report of a case with classic histologic, cytogenetics, and molecular genetic features. | journal=Am J Surg Pathol | year= 2008 | volume= 32 | issue= 6 | pages= 951-4 | pmid=18551755 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=18551755 }} &lt;/ref&gt;.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556365 2019-03-05T19:02:17Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Lipomas are defined as soft masses of adipose (fat) cells which are often encapsulated by a thin layer of fibrous tissue. <br /> *They are benign tumors of subcutaneous fat, not attached to the underlying fascia.<br /> *Clinically, they often present in the cephalic part of the body, specifically in the head, neck, shoulders, and backs of patients, although they can less commonly be seen elsewhere, for example, the thighs. <br /> *The tumors typically lie in the subcutaneous tissues of patients.<br /> *Lipomas can also arise in visceral organs such as stomach, liver, duodenum, colon, thyroid, adrenal glands, pancreas, and parathyroid glands.<br /> *Maxillofacial lipomas, including intralingual, parotid, orbitonasal, maxillary sinusoidal, and parapharyngeal space masses, have also been documented.<br /> *Gynecologic lipomas may occur in the uterus, ovaries, and broad ligament. <br /> *Involvement of the heart (causing ventricular tachycardia), superior vena cava, brain, and spinal cord may also occur.<br /> *Bone and intrarticular involvement is also common.<br /> *Mucosal lipoms in the gatsrointestnial tract can cause bleeding and intuscception.<br /> *Lipomas are histologically characterized by mature fat cells with no cytologic atypia/hyperchromasia/pleomorphism.<br /> *Lipoblasts can be seen in lipomas, but they do not exhibit cytologic atypia/hyperchromasia/pleomorphism.<br /> <br /> === Genetics ===<br /> * Lipomas are mainly characterized by rearrangements of chromosome 12q13q15 with several partner chromosomes in approximately, especially chromosome 3.<br /> * Lipomas without 12q13q15 rearrangements frequently show rearrangements of chromosome 6p21.<br /> * Several lipoma fusion genes have been identified and the most common is LPP-HMGA2, product of the t(3;12)(q27-q28;q14-a15). <br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_classification&diff=1556313 2019-03-05T18:18:53Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipoma may be classified into 12 subtypes: adenolipomas, angiolipoleiomyomas, [[angiolipoma]], cerebellar pontine angle and internal auditory canal lipomas, chondroid lipomas, [[corpus callosum]], hibernomas, intradermal spindle cell lipomas, neural fibrolipomas, pleomorphic lipomas, spindle-cell lipomas, and superficial subcutaneous lipomas.<br /> <br /> ==Classification==<br /> <br /> There are many subtypes of lipomas:&lt;ref name=&quot;Andrews&quot;&gt;{{cite book| edition = 10th| publisher = Elsevier| isbn = 0-7216-2921-0| last = James| first = William D.| first2 = Timothy G. |last2=Berger|first3= Dirk M.|last3= Elston| title = Andrews' Diseases of the Skin: Clinical Dermatology|location=London|year=2005}}&lt;/ref&gt;<br /> *'''Adenolipomas''' are lipomas associated with [[eccrine sweat glands]].&lt;ref name=&quot;Andrews new ed.&quot;&gt;{{cite book| edition = 11th| publisher = Elsevier| isbn = 9781437703146| last = James| first = William D.| first2 = Timothy G. |last2=Berger|first3= Dirk M.|last3= Elston| title = Andrews' Diseases of the Skin: Clinical Dermatology|location=London|year=2011}}&lt;/ref&gt;<br /> *'''Angiolipoleiomyomas''' are acquired, solitary, asymptomatic acral nodules, characterized histologically by well-circumscribed subcutaneous tumors composed of [[smooth muscle cells]], [[blood vessels]], [[connective tissue]], and fat.<br /> *'''[[Angiolipoma]]s''' painful subcutaneous nodules having all other features of a typical lipoma.&lt;ref name=&quot;Andrews&quot; /&gt;&lt;ref name=&quot;Bolognia&quot;&gt;{{cite book |author=Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. |title=Dermatology: 2-Volume Set |publisher=Mosby |location=St. Louis |year=2007 |pages=1838 |isbn=1-4160-2999-0 |oclc= |doi= |accessdate=}}&lt;/ref&gt;<br /> *'''Cerebellar pontine angle and internal auditory canal lipomas'''&lt;ref&gt;{{cite journal | author = Crowson MG, Symons SP, Chen JM | year = | title = Left cerebellopontine angle lipoma with mild brainstem compression in a 13-year-old female | url = | journal = Otology&amp; Neurotology | volume = | issue = | page = }}&lt;/ref&gt;<br /> *'''Chondroid lipomas''' are deep-seated, firm, yellow tumors that characteristically occur on the legs of women.<br /> *'''[[Corpus callosum]] lipoma''' is a rare congenital brain condition that may or may not present with symptoms.&lt;ref&gt;{{cite journal |author=Wallace D |title=Lipoma of the corpus callosum |journal=J Neurol Neurosurg Psychiatry. |volume=39 |issue=12 |pages=1179–85 |date=December 1976 |pmid=1011028 |pmc=492562 |doi= 10.1136/jnnp.39.12.1179|url=}}&lt;/ref&gt; This occurs in the corpus callosum, also known as the colossal commissure, which is a wide, flat bundle of neural fibers beneath the cortex in the human brain.<br /> *'''Hibernomas''' are lipoma of [[brown fat]].<br /> *'''Intradermal spindle cell lipomas''' are distinct in that they most commonly affect women and have a wide distribution, occurring with relatively equal frequency on the head and neck, trunk, and upper and lower extremities.&lt;ref name=&quot;Andrews&quot; /&gt;&lt;ref name=&quot;Bolognia&quot; /&gt;<br /> *'''Neural fibrolipomas''' are overgrowths of fibro-fatty tissue along a nerve trunk, which often leads to nerve compression.<br /> *'''Pleomorphic lipomas''', like spindle-cell lipomas, occur for the most part on the backs and necks of elderly men and are characterized by floret giant cells with overlapping nuclei.<br /> *'''Spindle-cell lipomas''' are asymptomatic, slow-growing subcutaneous tumors that have a predilection for the posterior back, neck, and shoulders of older men.<br /> *'''Superficial subcutaneous lipomas''', the most common type of lipoma, lie just below the surface of the skin. Most occur on the [[Torso|trunk]], [[thigh]], and [[forearm]], although they may be found anywhere in the body where fat is located.<br /> <br /> * <br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_classification&diff=1556312 2019-03-05T18:18:19Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipoma may be classified into 12 subtypes: adenolipomas, angiolipoleiomyomas, [[angiolipoma]], cerebellar pontine angle and internal auditory canal lipomas, chondroid lipomas, [[corpus callosum]], hibernomas, intradermal spindle cell lipomas, neural fibrolipomas, pleomorphic lipomas, spindle-cell lipomas, and superficial subcutaneous lipomas.<br /> <br /> ==Classification==<br /> * <br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Endocrinology]]<br /> [[Category:Surgery]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Lipoma_pathophysiology&diff=1556245 2019-03-05T16:54:42Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Lipoma}}<br /> <br /> {{CMG}}<br /> <br /> ==Overview==<br /> Lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. Solid components may present in some cases.<br /> <br /> ==Pathophysiology==<br /> <br /> *Simple lipomas are circumscribed encapsulated soft masses, made nearly entirely of fat. <br /> *Occasionally solid components will be present (blood vessels, muscle fibres, fibrous septae, and fat necrosis), which need to be carefully assessed to ensure that these do not represent a more aggressive component. <br /> *Histology demonstrates mature adipocytes with no cellular atypia or [[pleomorphism]].&lt;ref name=&quot;radio&quot;&gt;Lipoma.Dr Ahmed Abd Rabou and Dr Frank Gaillard, et al. Radiopaedia.org 2015.http://radiopaedia.org/articles/lipoma &lt;/ref&gt;<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> <br /> [[Category:Disease]]<br /> [[Category:Types of cancer]]<br /> [[Category:Surgery]]<br /> [[Category:Needs content]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546868 2019-02-07T04:55:17Z

<p>Jogeet singh sekhon: /* Differentiating Villous Adenoma from Other Diseases */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{JSS}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]]&lt;nowiki/&gt;transformation. Villous adenoma was first discovered by Helwig in 1946. Villous adenoma may be classified into flat, sessile, pedunculated and depressed subtypes. Villous adenoma arises from [[Epithelium|epithelial]] tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], STK11 and SMAD4. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]. Surgical removal is the mainstay of therapy for villous adenoma. Exploratory [[colonoscopy]] and [[Cauterization|cautery]] snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> [[Colon polyps|Colon polyp]]&lt;nowiki/&gt;s are classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *[[Tubular]]<br /> *Tubulovillous<br /> *[[Villous carcinoma|Villous]] <br /> Villous adenoma is classified into 4 types according to the gross appearance&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to [[dysplasia]]:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colon poylp&lt;ref name=&quot;pmid18314605&quot;&gt;{{cite journal |vauthors=Rüschoff J, Aust D, Hartmann A |title=[Colorectal serrated adenoma: diagnostic criteria and clinical implications] |language=German |journal=Verh Dtsch Ges Pathol |volume=91 |issue= |pages=119–25 |year=2007 |pmid=18314605 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;&lt;ref name=&quot;SinghZorrón Cheng Tao Pu2016&quot;&gt;{{cite journal|last1=Singh|first1=Rajvinder|last2=Zorrón Cheng Tao Pu|first2=Leonardo|last3=Koay|first3=Doreen|last4=Burt|first4=Alastair|title=Sessile serrated adenoma/polyps: Where are we at in 2016?|journal=World Journal of Gastroenterology|volume=22|issue=34|year=2016|pages=7754|issn=1007-9327|doi=10.3748/wjg.v22.i34.7754}}&lt;/ref&gt;&lt;ref name=&quot;KahiVemulapalli2015&quot;&gt;{{cite journal|last1=Kahi|first1=Charles J.|last2=Vemulapalli|first2=Krishna C.|last3=Snover|first3=Dale C.|last4=Abdel Jawad|first4=Khaled H.|last5=Cummings|first5=Oscar W.|last6=Rex|first6=Douglas K.|title=Findings in the Distal Colorectum Are Not Associated With Proximal Advanced Serrated Lesions|journal=Clinical Gastroenterology and Hepatology|volume=13|issue=2|year=2015|pages=345–351|issn=15423565|doi=10.1016/j.cgh.2014.07.044}}&lt;/ref&gt;.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * [[Dysplasia|Dysplastic]] changes are present in the adenomas.<br /> * Multiple genetic [[Mutation|mutations]] result in the transition from normal [[Mucous membrane|mucosa]] to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated [[Cell nucleus|nuclei]] which occupy the basal half of the [[cytoplasm]].&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** [[Pleomorphism]] and atypical [[Mitosis|mitoses]] are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the [[basement membrane]] into the [[lamina propria]]. <br /> ** As there are no [[Lymphatic system|lymphatic]] vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent [[nucleoli]]. <br /> ** Significant [[pleomorphism]], rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back [[glandular]] tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to [[adenocarcinoma]] of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of [[Oncogene|oncogenes]] and inactivation of [[Tumor suppressor gene|tumor suppresor genes]]&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** [[APC]] gene on 5 chromosome associated with [[FAP|familial automatosis polyposis]] syndrome and [[Gardner's syndrome|Gardner syndrome]]<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with [[Peutz-Jeghers syndrome]].<br /> ** SMAD4 on chromosome 8 associated with [[juvenile polyposis syndrome]].<br /> * Villous adenomas may cause secretory [[diarrhea]] characterized by [[hypokalemia]], chloride-rich stool, and [[metabolic alkalosis]]. Increased numbers of [[Goblet cell|goblet cells]] and increased [[Prostaglandin E2 receptor|prostaglandin E2]] are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> * Tubular adenoma<br /> * Tubulovillous adenoma<br /> * Hyperplastic polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide&lt;ref name=&quot;pmid15666099&quot;&gt;{{cite journal |vauthors=Giacosa A, Frascio F, Munizzi F |title=Epidemiology of colorectal polyps |journal=Tech Coloproctol |volume=8 Suppl 2 |issue= |pages=s243–7 |year=2004 |pmid=15666099 |doi=10.1007/s10151-004-0169-y |url=}}&lt;/ref&gt;. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas is common worldwide and has no regional predilection.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;&lt;ref name=&quot;pmid12376501&quot;&gt;{{cite journal |vauthors=Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD |title=Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential? |journal=Cancer Epidemiol. Biomarkers Prev. |volume=11 |issue=10 Pt 1 |pages=1012–8 |year=2002 |pmid=12376501 |doi= |url=}}&lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * [[Inflammatory bowel disease]]<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years&lt;ref name=&quot;Bonnington2016&quot;&gt;{{cite journal|last1=Bonnington|first1=Stewart N|title=Surveillance of colonic polyps: Are we getting it right?|journal=World Journal of Gastroenterology|volume=22|issue=6|year=2016|pages=1925|issn=1007-9327|doi=10.3748/wjg.v22.i6.1925}}&lt;/ref&gt;.<br /> * They are usually found accidentally on routine [[Colonoscopy|colonoscopic]] surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of [[colon polyps]].<br /> * Family history of [[Colorectal cancer|colon cancer]] or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *[[Bowel obstruction|Intestinal obstruction]]<br /> *Progression to [[colorectal cancer]].<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%&lt;ref name=&quot;BettingtonWalker2013&quot;&gt;{{cite journal|last1=Bettington|first1=Mark|last2=Walker|first2=Neal|last3=Clouston|first3=Andrew|last4=Brown|first4=Ian|last5=Leggett|first5=Barbara|last6=Whitehall|first6=Vicki|title=The serrated pathway to colorectal carcinoma: current concepts and challenges|journal=Histopathology|volume=62|issue=3|year=2013|pages=367–386|issn=03090167|doi=10.1111/his.12055}}&lt;/ref&gt; .<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * [[Biopsy]] of the lesion is the diagnostic study of choice&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms&lt;ref name=&quot;JohnsonKisiel2017&quot;&gt;{{cite journal|last1=Johnson|first1=David H.|last2=Kisiel|first2=John B.|last3=Burger|first3=Kelli N.|last4=Mahoney|first4=Douglas W.|last5=Devens|first5=Mary E.|last6=Ahlquist|first6=David A.|last7=Sweetser|first7=Seth|title=Multitarget stool DNA test: clinical performance and impact on yield and quality of colonoscopy for colorectal cancer screening|journal=Gastrointestinal Endoscopy|volume=85|issue=3|year=2017|pages=657–665.e1|issn=00165107|doi=10.1016/j.gie.2016.11.012}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;<br /> =:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *[[Gastrointestinal bleeding|Blood in stools]]<br /> *[[Weight loss]]<br /> *Change in bowel habits<br /> *[[Fatigue]]<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *[[Pallor]] due to [[Occult blood|occult]] bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *[[Rectal masses|Rectal mass]] on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive [[fecal occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * [[Anemia]]<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and [[sigmoidoscopy]], villous adenoma is visualised as a [[polyp]].<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, [[aspirin]] 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer&lt;ref name=&quot;pmid27064573&quot;&gt;{{cite journal |vauthors=Dehmer SP, Maciosek MV, Flottemesch TJ, LaFrance AB, Whitlock EP |title=Aspirin for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: A Decision Analysis for the U.S. Preventive Services Task Force |journal=Ann. Intern. Med. |volume=164 |issue=12 |pages=777–86 |year=2016 |pmid=27064573 |doi=10.7326/M15-2129 |url=}}&lt;/ref&gt;.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma&lt;ref name=&quot;Winawer2015&quot;&gt;{{cite journal|last1=Winawer|first1=Sidney J.|title=The History of Colorectal Cancer Screening: A Personal Perspective|journal=Digestive Diseases and Sciences|volume=60|issue=3|year=2015|pages=596–608|issn=0163-2116|doi=10.1007/s10620-014-3466-y}}&lt;/ref&gt;&lt;ref name=&quot;RameshshankerWilson2016&quot;&gt;{{cite journal|last1=Rameshshanker|first1=R.|last2=Wilson|first2=Ana|title=Electronic Imaging in Colonoscopy: Clinical Applications and Future Prospects|journal=Current Treatment Options in Gastroenterology|volume=14|issue=1|year=2016|pages=140–151|issn=1092-8472|doi=10.1007/s11938-016-0075-1}}&lt;/ref&gt;.<br /> * The removal of adenoma is known as [[polypectomy]] and is done through colonoscopy by endoscopic forceps snare.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include: <br /> * Periodic screening for polyps in patients with family history of : <br /> ** [[Familial adenomatous polyposis]] <br /> ** [[Peutz–Jeghers syndrome]]<br /> ** [[Turcot syndrome]]<br /> ** [[Juvenile polyposis syndrome]]<br /> ** [[Cowden disease]]<br /> ** [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> ** [[Gardner's syndrome]]<br /> * Exercise<br /> * Smoking cessation<br /> * Avoid alcohol<br /> * High fiber diet<br /> <br /> ====Secondary Prevention====<br /> Aspirin 75mg PO daily.<br /> * Annual [[occult blood test]]&lt;ref name=&quot;pmid22763141&quot;&gt;{{cite journal| author=Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR| title=Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. | journal=Gastroenterology | year= 2012 | volume= 143 | issue= 3 | pages= 844-857 | pmid=22763141 | doi=10.1053/j.gastro.2012.06.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22763141 }} &lt;/ref&gt;<br /> * Colonoscopy every ten years for patients above the age of 50 with no family history of colon cancer or no history of colon polyps.<br /> * Colonoscopy at the age of 40 or 10 years before the age of cancer diagnosis in a relative with colon cancer and repeat every 3-5 years.<br /> * Colonoscopy after polypectomy:<br /> ** Every 5 years if 1-2 adenomas present or size &lt;1 cm.<br /> ** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm.<br /> ** Every 1-2 years if &gt;10 adenomas present or if size is &gt;2cm.<br /> ** Every 2-6 months if signs of adenocarcinoma present.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546867 2019-02-07T04:51:18Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{JSS}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]]&lt;nowiki/&gt;transformation. Villous adenoma was first discovered by Helwig in 1946. Villous adenoma may be classified into flat, sessile, pedunculated and depressed subtypes. Villous adenoma arises from [[Epithelium|epithelial]] tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], STK11 and SMAD4. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]. Surgical removal is the mainstay of therapy for villous adenoma. Exploratory [[colonoscopy]] and [[Cauterization|cautery]] snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> [[Colon polyps|Colon polyp]]&lt;nowiki/&gt;s are classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *[[Tubular]]<br /> *Tubulovillous<br /> *[[Villous carcinoma|Villous]] <br /> Villous adenoma is classified into 4 types according to the gross appearance&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to [[dysplasia]]:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colon poylp&lt;ref name=&quot;pmid18314605&quot;&gt;{{cite journal |vauthors=Rüschoff J, Aust D, Hartmann A |title=[Colorectal serrated adenoma: diagnostic criteria and clinical implications] |language=German |journal=Verh Dtsch Ges Pathol |volume=91 |issue= |pages=119–25 |year=2007 |pmid=18314605 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;&lt;ref name=&quot;SinghZorrón Cheng Tao Pu2016&quot;&gt;{{cite journal|last1=Singh|first1=Rajvinder|last2=Zorrón Cheng Tao Pu|first2=Leonardo|last3=Koay|first3=Doreen|last4=Burt|first4=Alastair|title=Sessile serrated adenoma/polyps: Where are we at in 2016?|journal=World Journal of Gastroenterology|volume=22|issue=34|year=2016|pages=7754|issn=1007-9327|doi=10.3748/wjg.v22.i34.7754}}&lt;/ref&gt;&lt;ref name=&quot;KahiVemulapalli2015&quot;&gt;{{cite journal|last1=Kahi|first1=Charles J.|last2=Vemulapalli|first2=Krishna C.|last3=Snover|first3=Dale C.|last4=Abdel Jawad|first4=Khaled H.|last5=Cummings|first5=Oscar W.|last6=Rex|first6=Douglas K.|title=Findings in the Distal Colorectum Are Not Associated With Proximal Advanced Serrated Lesions|journal=Clinical Gastroenterology and Hepatology|volume=13|issue=2|year=2015|pages=345–351|issn=15423565|doi=10.1016/j.cgh.2014.07.044}}&lt;/ref&gt;.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * [[Dysplasia|Dysplastic]] changes are present in the adenomas.<br /> * Multiple genetic [[Mutation|mutations]] result in the transition from normal [[Mucous membrane|mucosa]] to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated [[Cell nucleus|nuclei]] which occupy the basal half of the [[cytoplasm]].&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** [[Pleomorphism]] and atypical [[Mitosis|mitoses]] are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the [[basement membrane]] into the [[lamina propria]]. <br /> ** As there are no [[Lymphatic system|lymphatic]] vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent [[nucleoli]]. <br /> ** Significant [[pleomorphism]], rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back [[glandular]] tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to [[adenocarcinoma]] of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of [[Oncogene|oncogenes]] and inactivation of [[Tumor suppressor gene|tumor suppresor genes]]&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** [[APC]] gene on 5 chromosome associated with [[FAP|familial automatosis polyposis]] syndrome and [[Gardner's syndrome|Gardner syndrome]]<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with [[Peutz-Jeghers syndrome]].<br /> ** SMAD4 on chromosome 8 associated with [[juvenile polyposis syndrome]].<br /> * Villous adenomas may cause secretory [[diarrhea]] characterized by [[hypokalemia]], chloride-rich stool, and [[metabolic alkalosis]]. Increased numbers of [[Goblet cell|goblet cells]] and increased [[Prostaglandin E2 receptor|prostaglandin E2]] are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide&lt;ref name=&quot;pmid15666099&quot;&gt;{{cite journal |vauthors=Giacosa A, Frascio F, Munizzi F |title=Epidemiology of colorectal polyps |journal=Tech Coloproctol |volume=8 Suppl 2 |issue= |pages=s243–7 |year=2004 |pmid=15666099 |doi=10.1007/s10151-004-0169-y |url=}}&lt;/ref&gt;. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas is common worldwide and has no regional predilection.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;&lt;ref name=&quot;pmid12376501&quot;&gt;{{cite journal |vauthors=Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD |title=Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential? |journal=Cancer Epidemiol. Biomarkers Prev. |volume=11 |issue=10 Pt 1 |pages=1012–8 |year=2002 |pmid=12376501 |doi= |url=}}&lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * [[Inflammatory bowel disease]]<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years&lt;ref name=&quot;Bonnington2016&quot;&gt;{{cite journal|last1=Bonnington|first1=Stewart N|title=Surveillance of colonic polyps: Are we getting it right?|journal=World Journal of Gastroenterology|volume=22|issue=6|year=2016|pages=1925|issn=1007-9327|doi=10.3748/wjg.v22.i6.1925}}&lt;/ref&gt;.<br /> * They are usually found accidentally on routine [[Colonoscopy|colonoscopic]] surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of [[colon polyps]].<br /> * Family history of [[Colorectal cancer|colon cancer]] or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *[[Bowel obstruction|Intestinal obstruction]]<br /> *Progression to [[colorectal cancer]].<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%&lt;ref name=&quot;BettingtonWalker2013&quot;&gt;{{cite journal|last1=Bettington|first1=Mark|last2=Walker|first2=Neal|last3=Clouston|first3=Andrew|last4=Brown|first4=Ian|last5=Leggett|first5=Barbara|last6=Whitehall|first6=Vicki|title=The serrated pathway to colorectal carcinoma: current concepts and challenges|journal=Histopathology|volume=62|issue=3|year=2013|pages=367–386|issn=03090167|doi=10.1111/his.12055}}&lt;/ref&gt; .<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * [[Biopsy]] of the lesion is the diagnostic study of choice&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms&lt;ref name=&quot;JohnsonKisiel2017&quot;&gt;{{cite journal|last1=Johnson|first1=David H.|last2=Kisiel|first2=John B.|last3=Burger|first3=Kelli N.|last4=Mahoney|first4=Douglas W.|last5=Devens|first5=Mary E.|last6=Ahlquist|first6=David A.|last7=Sweetser|first7=Seth|title=Multitarget stool DNA test: clinical performance and impact on yield and quality of colonoscopy for colorectal cancer screening|journal=Gastrointestinal Endoscopy|volume=85|issue=3|year=2017|pages=657–665.e1|issn=00165107|doi=10.1016/j.gie.2016.11.012}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;<br /> =:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *[[Gastrointestinal bleeding|Blood in stools]]<br /> *[[Weight loss]]<br /> *Change in bowel habits<br /> *[[Fatigue]]<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *[[Pallor]] due to [[Occult blood|occult]] bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *[[Rectal masses|Rectal mass]] on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive [[fecal occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * [[Anemia]]<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and [[sigmoidoscopy]], villous adenoma is visualised as a [[polyp]].<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, [[aspirin]] 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer&lt;ref name=&quot;pmid27064573&quot;&gt;{{cite journal |vauthors=Dehmer SP, Maciosek MV, Flottemesch TJ, LaFrance AB, Whitlock EP |title=Aspirin for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: A Decision Analysis for the U.S. Preventive Services Task Force |journal=Ann. Intern. Med. |volume=164 |issue=12 |pages=777–86 |year=2016 |pmid=27064573 |doi=10.7326/M15-2129 |url=}}&lt;/ref&gt;.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma&lt;ref name=&quot;Winawer2015&quot;&gt;{{cite journal|last1=Winawer|first1=Sidney J.|title=The History of Colorectal Cancer Screening: A Personal Perspective|journal=Digestive Diseases and Sciences|volume=60|issue=3|year=2015|pages=596–608|issn=0163-2116|doi=10.1007/s10620-014-3466-y}}&lt;/ref&gt;&lt;ref name=&quot;RameshshankerWilson2016&quot;&gt;{{cite journal|last1=Rameshshanker|first1=R.|last2=Wilson|first2=Ana|title=Electronic Imaging in Colonoscopy: Clinical Applications and Future Prospects|journal=Current Treatment Options in Gastroenterology|volume=14|issue=1|year=2016|pages=140–151|issn=1092-8472|doi=10.1007/s11938-016-0075-1}}&lt;/ref&gt;.<br /> * The removal of adenoma is known as [[polypectomy]] and is done through colonoscopy by endoscopic forceps snare.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include: <br /> * Periodic screening for polyps in patients with family history of : <br /> ** [[Familial adenomatous polyposis]] <br /> ** [[Peutz–Jeghers syndrome]]<br /> ** [[Turcot syndrome]]<br /> ** [[Juvenile polyposis syndrome]]<br /> ** [[Cowden disease]]<br /> ** [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> ** [[Gardner's syndrome]]<br /> * Exercise<br /> * Smoking cessation<br /> * Avoid alcohol<br /> * High fiber diet<br /> <br /> ====Secondary Prevention====<br /> Aspirin 75mg PO daily.<br /> * Annual [[occult blood test]]&lt;ref name=&quot;pmid22763141&quot;&gt;{{cite journal| author=Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR| title=Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. | journal=Gastroenterology | year= 2012 | volume= 143 | issue= 3 | pages= 844-857 | pmid=22763141 | doi=10.1053/j.gastro.2012.06.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22763141 }} &lt;/ref&gt;<br /> * Colonoscopy every ten years for patients above the age of 50 with no family history of colon cancer or no history of colon polyps.<br /> * Colonoscopy at the age of 40 or 10 years before the age of cancer diagnosis in a relative with colon cancer and repeat every 3-5 years.<br /> * Colonoscopy after polypectomy:<br /> ** Every 5 years if 1-2 adenomas present or size &lt;1 cm.<br /> ** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm.<br /> ** Every 1-2 years if &gt;10 adenomas present or if size is &gt;2cm.<br /> ** Every 2-6 months if signs of adenocarcinoma present.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546866 2019-02-07T04:50:12Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]]&lt;nowiki/&gt;transformation. Villous adenoma was first discovered by Helwig in 1946. Villous adenoma may be classified into flat, sessile, pedunculated and depressed subtypes. Villous adenoma arises from [[Epithelium|epithelial]] tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], STK11 and SMAD4. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]. Surgical removal is the mainstay of therapy for villous adenoma. Exploratory [[colonoscopy]] and [[Cauterization|cautery]] snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> [[Colon polyps|Colon polyp]]&lt;nowiki/&gt;s are classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *[[Tubular]]<br /> *Tubulovillous<br /> *[[Villous carcinoma|Villous]] <br /> Villous adenoma is classified into 4 types according to the gross appearance&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to [[dysplasia]]:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colon poylp&lt;ref name=&quot;pmid18314605&quot;&gt;{{cite journal |vauthors=Rüschoff J, Aust D, Hartmann A |title=[Colorectal serrated adenoma: diagnostic criteria and clinical implications] |language=German |journal=Verh Dtsch Ges Pathol |volume=91 |issue= |pages=119–25 |year=2007 |pmid=18314605 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;&lt;ref name=&quot;SinghZorrón Cheng Tao Pu2016&quot;&gt;{{cite journal|last1=Singh|first1=Rajvinder|last2=Zorrón Cheng Tao Pu|first2=Leonardo|last3=Koay|first3=Doreen|last4=Burt|first4=Alastair|title=Sessile serrated adenoma/polyps: Where are we at in 2016?|journal=World Journal of Gastroenterology|volume=22|issue=34|year=2016|pages=7754|issn=1007-9327|doi=10.3748/wjg.v22.i34.7754}}&lt;/ref&gt;&lt;ref name=&quot;KahiVemulapalli2015&quot;&gt;{{cite journal|last1=Kahi|first1=Charles J.|last2=Vemulapalli|first2=Krishna C.|last3=Snover|first3=Dale C.|last4=Abdel Jawad|first4=Khaled H.|last5=Cummings|first5=Oscar W.|last6=Rex|first6=Douglas K.|title=Findings in the Distal Colorectum Are Not Associated With Proximal Advanced Serrated Lesions|journal=Clinical Gastroenterology and Hepatology|volume=13|issue=2|year=2015|pages=345–351|issn=15423565|doi=10.1016/j.cgh.2014.07.044}}&lt;/ref&gt;.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * [[Dysplasia|Dysplastic]] changes are present in the adenomas.<br /> * Multiple genetic [[Mutation|mutations]] result in the transition from normal [[Mucous membrane|mucosa]] to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated [[Cell nucleus|nuclei]] which occupy the basal half of the [[cytoplasm]].&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** [[Pleomorphism]] and atypical [[Mitosis|mitoses]] are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the [[basement membrane]] into the [[lamina propria]]. <br /> ** As there are no [[Lymphatic system|lymphatic]] vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent [[nucleoli]]. <br /> ** Significant [[pleomorphism]], rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back [[glandular]] tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to [[adenocarcinoma]] of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of [[Oncogene|oncogenes]] and inactivation of [[Tumor suppressor gene|tumor suppresor genes]]&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** [[APC]] gene on 5 chromosome associated with [[FAP|familial automatosis polyposis]] syndrome and [[Gardner's syndrome|Gardner syndrome]]<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with [[Peutz-Jeghers syndrome]].<br /> ** SMAD4 on chromosome 8 associated with [[juvenile polyposis syndrome]].<br /> * Villous adenomas may cause secretory [[diarrhea]] characterized by [[hypokalemia]], chloride-rich stool, and [[metabolic alkalosis]]. Increased numbers of [[Goblet cell|goblet cells]] and increased [[Prostaglandin E2 receptor|prostaglandin E2]] are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide&lt;ref name=&quot;pmid15666099&quot;&gt;{{cite journal |vauthors=Giacosa A, Frascio F, Munizzi F |title=Epidemiology of colorectal polyps |journal=Tech Coloproctol |volume=8 Suppl 2 |issue= |pages=s243–7 |year=2004 |pmid=15666099 |doi=10.1007/s10151-004-0169-y |url=}}&lt;/ref&gt;. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas is common worldwide and has no regional predilection.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;&lt;ref name=&quot;pmid12376501&quot;&gt;{{cite journal |vauthors=Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD |title=Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential? |journal=Cancer Epidemiol. Biomarkers Prev. |volume=11 |issue=10 Pt 1 |pages=1012–8 |year=2002 |pmid=12376501 |doi= |url=}}&lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * [[Inflammatory bowel disease]]<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years&lt;ref name=&quot;Bonnington2016&quot;&gt;{{cite journal|last1=Bonnington|first1=Stewart N|title=Surveillance of colonic polyps: Are we getting it right?|journal=World Journal of Gastroenterology|volume=22|issue=6|year=2016|pages=1925|issn=1007-9327|doi=10.3748/wjg.v22.i6.1925}}&lt;/ref&gt;.<br /> * They are usually found accidentally on routine [[Colonoscopy|colonoscopic]] surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of [[colon polyps]].<br /> * Family history of [[Colorectal cancer|colon cancer]] or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *[[Bowel obstruction|Intestinal obstruction]]<br /> *Progression to [[colorectal cancer]].<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%&lt;ref name=&quot;BettingtonWalker2013&quot;&gt;{{cite journal|last1=Bettington|first1=Mark|last2=Walker|first2=Neal|last3=Clouston|first3=Andrew|last4=Brown|first4=Ian|last5=Leggett|first5=Barbara|last6=Whitehall|first6=Vicki|title=The serrated pathway to colorectal carcinoma: current concepts and challenges|journal=Histopathology|volume=62|issue=3|year=2013|pages=367–386|issn=03090167|doi=10.1111/his.12055}}&lt;/ref&gt; .<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * [[Biopsy]] of the lesion is the diagnostic study of choice&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms&lt;ref name=&quot;JohnsonKisiel2017&quot;&gt;{{cite journal|last1=Johnson|first1=David H.|last2=Kisiel|first2=John B.|last3=Burger|first3=Kelli N.|last4=Mahoney|first4=Douglas W.|last5=Devens|first5=Mary E.|last6=Ahlquist|first6=David A.|last7=Sweetser|first7=Seth|title=Multitarget stool DNA test: clinical performance and impact on yield and quality of colonoscopy for colorectal cancer screening|journal=Gastrointestinal Endoscopy|volume=85|issue=3|year=2017|pages=657–665.e1|issn=00165107|doi=10.1016/j.gie.2016.11.012}}&lt;/ref&gt;&lt;ref name=&quot;ShussmanWexner2014&quot;&gt;{{cite journal|last1=Shussman|first1=N.|last2=Wexner|first2=S. D.|title=Colorectal polyps and polyposis syndromes|journal=Gastroenterology Report|volume=2|issue=1|year=2014|pages=1–15|issn=2052-0034|doi=10.1093/gastro/got041}}&lt;/ref&gt;<br /> =:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *[[Gastrointestinal bleeding|Blood in stools]]<br /> *[[Weight loss]]<br /> *Change in bowel habits<br /> *[[Fatigue]]<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *[[Pallor]] due to [[Occult blood|occult]] bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *[[Rectal masses|Rectal mass]] on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive [[fecal occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * [[Anemia]]<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and [[sigmoidoscopy]], villous adenoma is visualised as a [[polyp]].<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, [[aspirin]] 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer&lt;ref name=&quot;pmid27064573&quot;&gt;{{cite journal |vauthors=Dehmer SP, Maciosek MV, Flottemesch TJ, LaFrance AB, Whitlock EP |title=Aspirin for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: A Decision Analysis for the U.S. Preventive Services Task Force |journal=Ann. Intern. Med. |volume=164 |issue=12 |pages=777–86 |year=2016 |pmid=27064573 |doi=10.7326/M15-2129 |url=}}&lt;/ref&gt;.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma&lt;ref name=&quot;Winawer2015&quot;&gt;{{cite journal|last1=Winawer|first1=Sidney J.|title=The History of Colorectal Cancer Screening: A Personal Perspective|journal=Digestive Diseases and Sciences|volume=60|issue=3|year=2015|pages=596–608|issn=0163-2116|doi=10.1007/s10620-014-3466-y}}&lt;/ref&gt;&lt;ref name=&quot;RameshshankerWilson2016&quot;&gt;{{cite journal|last1=Rameshshanker|first1=R.|last2=Wilson|first2=Ana|title=Electronic Imaging in Colonoscopy: Clinical Applications and Future Prospects|journal=Current Treatment Options in Gastroenterology|volume=14|issue=1|year=2016|pages=140–151|issn=1092-8472|doi=10.1007/s11938-016-0075-1}}&lt;/ref&gt;.<br /> * The removal of adenoma is known as [[polypectomy]] and is done through colonoscopy by endoscopic forceps snare.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include: <br /> * Periodic screening for polyps in patients with family history of : <br /> ** [[Familial adenomatous polyposis]] <br /> ** [[Peutz–Jeghers syndrome]]<br /> ** [[Turcot syndrome]]<br /> ** [[Juvenile polyposis syndrome]]<br /> ** [[Cowden disease]]<br /> ** [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> ** [[Gardner's syndrome]]<br /> * Exercise<br /> * Smoking cessation<br /> * Avoid alcohol<br /> * High fiber diet<br /> <br /> ====Secondary Prevention====<br /> Aspirin 75mg PO daily.<br /> * Annual [[occult blood test]]&lt;ref name=&quot;pmid22763141&quot;&gt;{{cite journal| author=Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR| title=Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. | journal=Gastroenterology | year= 2012 | volume= 143 | issue= 3 | pages= 844-857 | pmid=22763141 | doi=10.1053/j.gastro.2012.06.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22763141 }} &lt;/ref&gt;<br /> * Colonoscopy every ten years for patients above the age of 50 with no family history of colon cancer or no history of colon polyps.<br /> * Colonoscopy at the age of 40 or 10 years before the age of cancer diagnosis in a relative with colon cancer and repeat every 3-5 years.<br /> * Colonoscopy after polypectomy:<br /> ** Every 5 years if 1-2 adenomas present or size &lt;1 cm.<br /> ** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm.<br /> ** Every 1-2 years if &gt;10 adenomas present or if size is &gt;2cm.<br /> ** Every 2-6 months if signs of adenocarcinoma present.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546865 2019-02-07T04:29:42Z

<p>Jogeet singh sekhon: /* Overview */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]]&lt;nowiki/&gt;transformation. Villous adenoma was first discovered by Helwig in 1946. Villous adenoma may be classified into flat, sessile, pedunculated and depressed subtypes. Villous adenoma arises from [[Epithelium|epithelial]] tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], STK11 and SMAD4. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]. Surgical removal is the mainstay of therapy for villous adenoma. Exploratory [[colonoscopy]] and [[Cauterization|cautery]] snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> [[Colon polyps|Colon polyp]]&lt;nowiki/&gt;s are classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *[[Tubular]]<br /> *Tubulovillous<br /> *[[Villous carcinoma|Villous]] <br /> Villous adenoma is classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to [[dysplasia]]:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colon poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * [[Dysplasia|Dysplastic]] changes are present in the adenomas.<br /> * Multiple genetic [[Mutation|mutations]] result in the transition from normal [[Mucous membrane|mucosa]] to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated [[Cell nucleus|nuclei]] which occupy the basal half of the [[cytoplasm]].&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** [[Pleomorphism]] and atypical [[Mitosis|mitoses]] are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the [[basement membrane]] into the [[lamina propria]]. <br /> ** As there are no [[Lymphatic system|lymphatic]] vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent [[nucleoli]]. <br /> ** Significant [[pleomorphism]], rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back [[glandular]] tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to [[adenocarcinoma]] of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of [[Oncogene|oncogenes]] and inactivation of [[Tumor suppressor gene|tumor suppresor genes]]&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** [[APC]] gene on 5 chromosome associated with [[FAP|familial automatosis polyposis]] syndrome and [[Gardner's syndrome|Gardner syndrome]]<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with [[Peutz-Jeghers syndrome]].<br /> ** SMAD4 on chromosome 8 associated with [[juvenile polyposis syndrome]].<br /> * Villous adenomas may cause secretory [[diarrhea]] characterized by [[hypokalemia]], chloride-rich stool, and [[metabolic alkalosis]]. Increased numbers of [[Goblet cell|goblet cells]] and increased [[Prostaglandin E2 receptor|prostaglandin E2]] are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas is common worldwide and has no regional predilection.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * [[Inflammatory bowel disease]]<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years.<br /> * They are usually found accidentally on routine [[Colonoscopy|colonoscopic]] surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of [[colon polyps]].<br /> * Family history of [[Colorectal cancer|colon cancer]] or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *[[Bowel obstruction|Intestinal obstruction]]<br /> *Progression to [[colorectal cancer]].<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%.<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * [[Biopsy]] of the lesion is the diagnostic study of choice.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *[[Gastrointestinal bleeding|Blood in stools]]<br /> *[[Weight loss]]<br /> *Change in bowel habits<br /> *[[Fatigue]]<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *[[Pallor]] due to [[Occult blood|occult]] bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *[[Rectal masses|Rectal mass]] on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive [[fecal occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * [[Anemia]]<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and [[sigmoidoscopy]], villous adenoma is visualised as a [[polyp]].<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, [[aspirin]] 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma.<br /> * The removal of adenoma is known as [[polypectomy]] and is done through colonoscopy by endoscopic forceps snare.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include: <br /> * Periodic screening for polyps in patients with family history of : <br /> ** [[Familial adenomatous polyposis]] <br /> ** [[Peutz–Jeghers syndrome]]<br /> ** [[Turcot syndrome]]<br /> ** [[Juvenile polyposis syndrome]]<br /> ** [[Cowden disease]]<br /> ** [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> ** [[Gardner's syndrome]]<br /> * Exercise<br /> * Smoking cessation<br /> * Avoid alcohol<br /> * High fiber diet<br /> <br /> ====Secondary Prevention====<br /> * Annual [[occult blood test]]<br /> * Colonoscopy every ten years for patients above the age of 50 with no family history of colon cancer or no history of colon polyps.<br /> * Colonoscopy at the age of 40 or 10 years before the age of cancer diagnosis in a relative with colon cancer and repeat every 3-5 years.<br /> * Colonoscopy after polypectomy:<br /> ** Every 5 years if 1-2 adenomas present or size &lt;1 cm.<br /> ** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm.<br /> ** Every 1-2 years if &gt;10 adenomas present or if size is &gt;2cm.<br /> ** Every 2-6 months if signs of adenocarcinoma present.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546863 2019-02-07T04:04:31Z

<p>Jogeet singh sekhon: /* Primary Prevention */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas are common worldwide.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * Inflammatory bowel disease<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years.<br /> * They are usually found accidentally on routine colonoscopic surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of colonic poylps.<br /> * Family history of colon cancer or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *Intestinal obstruction<br /> *Bowel torsion<br /> *Progression to colorectal cancer.<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%.<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * Biopsy of the lesion is the diagnostic study of choice.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Blood in stools<br /> *Weight loss<br /> *Change in bowel habits<br /> *Fatigue<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *Pallor due to occult bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *Rectal mass on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive fecal [[occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * Anemia<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and sigmoidoscopy, villous adenoma is visualised as a polyp.<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, aspirin 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma.<br /> * The removal of adenoma is known as polypectomy and is done through colonoscopy.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include: <br /> * Periodic screening for polyps in patients with family history of : <br /> ** [[Familial adenomatous polyposis]] <br /> ** [[Peutz–Jeghers syndrome]]<br /> ** [[Turcot syndrome]]<br /> ** [[Juvenile polyposis syndrome]]<br /> ** [[Cowden disease]]<br /> ** [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> ** [[Gardner's syndrome]]<br /> * Exercise<br /> * Smoking cessation<br /> * Avoid alcohol<br /> * High fiber diet<br /> <br /> ====Secondary Prevention====<br /> * Annual [[occult blood test]]<br /> * Colonoscopy every ten years for patients above the age of 50 with no family history of colon cancer or no history of colon polyps.<br /> * Colonoscopy at the age of 40 or 10 years before the age of cancer diagnosis in a relative with colon cancer and repeat every 3-5 years.<br /> * Colonoscopy after polypectomy:<br /> ** Every 5 years if 1-2 adenomas present or size &lt;1 cm.<br /> ** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm.<br /> ** Every 1-2 years if &gt;10 adenomas present or if size is &gt;2cm.<br /> ** Every 2-6 months if signs of adenocarcinoma present.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546856 2019-02-07T03:39:55Z

<p>Jogeet singh sekhon: /* Causes */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> The cause of villous adneoma is not yet identified.<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> * The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. <br /> <br /> ===Age===<br /> * Patients of all age groups may develop villous adenoma but the risk increases with age.<br /> <br /> ===Gender===<br /> * Males are more commonly affected with villous adenoma than females. <br /> <br /> ===Race===<br /> * African Americans are more prone to develop villous adneoma.<br /> <br /> === Region ===<br /> * Villous adenomas are common worldwide.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * Age more than 50 years.<br /> * African American race<br /> * Male sex<br /> * Inflammatory bowel disease<br /> * [[Alcoholism|Alcohol abuse]]<br /> * [[Obesity]]<br /> * Lack of [[Physical exercise|exercise]]<br /> * [[Diet (nutrition)|Diet]] high in red meats and processed meats<br /> * Low [[Fiber (food)|fiber]] intake<br /> * Low [[calcium]] intake<br /> * Low [[Folic Acid|folate]] intake<br /> * [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> * The majority of patients with villous adenoma remain asymptomatic for years.<br /> * They are usually found accidentally on routine colonoscopic surveillance.<br /> * Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].<br /> * If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * The patients may have a previous history of colonic poylps.<br /> * Family history of colon cancer or colon polyps.<br /> * History of smoking.<br /> <br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding|Gatsrointestinal Bleeding]]<br /> *Intestinal obstruction<br /> *Bowel torsion<br /> *Progression to colorectal cancer.<br /> <br /> ===Prognosis===<br /> * The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%.<br /> * Prognosis becomes poor with malignant transformation of the lesion. <br /> * Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.<br /> <br /> == Diagnosis ==<br /> <br /> === Diagnostic study of choice ===<br /> * Biopsy of the lesion is the diagnostic study of choice.<br /> * Villous adenoma is detected on colonoscopy or sigmoidoscopy.<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Blood in stools<br /> *Weight loss<br /> *Change in bowel habits<br /> *Fatigue<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma usually appear well but may have the following signs on exmaination.<br /> *Pallor due to occult bleeding<br /> *Abdominal tenderness <br /> *Bright red blood on digital rectal examination<br /> *Rectal mass on digital rectal examination<br /> <br /> === Laboratory Findings ===<br /> Laboratory findings associated with villous adenoma are:<br /> * Positive fecal [[occult blood test]]<br /> * H[[hypokalemia|ypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> * Anemia<br /> <br /> ===Other diagnostic studies===<br /> On [[colonoscopy]] and sigmoidoscopy, villous adenoma is visualised as a polyp.<br /> <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] <br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> * There is no medical therapy for villous adenoma.<br /> * Surgical removal of the adenoma is the mainstay of treatment.<br /> * However, aspirin 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer.<br /> <br /> === Surgery ===<br /> * Surgical removal is the mainstay of therapy for villous adenoma.<br /> * The removal of adenoma is known as polypectomy and is done through colonoscopy.<br /> * The removed adenoma is sent for biopsy.<br /> * <br /> {{#ev:youtube|ClgRkyhaJZw}}<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546829 2019-02-07T02:50:06Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea.<br /> [[Image:Colon_adenoma_(1).jpg|thumb|left|[[Colon (anatomy)|Colon]] [[adenoma]] By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=444694]]<br /> &lt;br style=&quot;clear:left&quot; /&gt;<br /> <br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546825 2019-02-07T02:46:06Z

<p>Jogeet singh sekhon: /* Pathophysiology */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea.<br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546824 2019-02-07T02:43:22Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea. <br /> <br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546823 2019-02-07T02:39:39Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance:<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> Villous adenoma is classified into 2 types according to dysplasia:<br /> * Low grade dysplasia<br /> * High grade dysplasia<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * Villous adenoma is a type of colonic poylp.<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.<br /> * Features of low grade dysplasia are:<br /> ** The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> ** Pleomorphism and atypical mitoses are absent.<br /> ** The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> ** As there are no lymphatic vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.<br /> * Features of high grade dysplasia are:<br /> ** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli. <br /> ** Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> ** The crypts are cribriform and crowded with back-to-back glandular tissue &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> ** These adenomas have a significant risk of metasstasis as the lesions can invade into the lamina propria through basement membrane destruction.<br /> * Villous adenoma can lead to adenocarcinoma of the colon.<br /> * The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppresor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The genes involved in adenoma formation are:<br /> ** K-ras oncogene <br /> ** Tumor suppresor p53 gene<br /> ** APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome<br /> ** [[STK11]] (LBK1) gene, located on [[chromosome]] 19 associated with Peutz-Jeghers syndrome.<br /> ** SMAD4 on chromosome 8 associated with juvenile polyposis syndrome.<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea. <br /> {|<br /> |[[Image:Villous_adenoma_of_the_sigmoid_colon,_gross_pathology.jpg|thumb|left|Villous [[Adenoma]] of the [[Transverse colon]] By http://web2.airmail.net/uthman/specimens/index.html, Public Domain, https://commons.wikimedia.org/w/index.php?curid=840194]]<br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546108 2019-02-06T03:42:10Z

<p>Jogeet singh sekhon: /* Pathophysiology */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Villous adenoma may be classified into 3 subtypes according to histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance.<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma.<br /> * The cytological features of low-grade dysplasia include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.&lt;ref name=&quot;pmid12725874&quot;&gt;{{cite journal| author=Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G et al.| title=Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC). | journal=J Clin Epidemiol | year= 2003 | volume= 56 | issue= 3 | pages= 209-14 | pmid=12725874 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12725874 }} &lt;/ref&gt;<br /> * Pleomorphism and atypical mitoses are absent in low grade dysplasia.<br /> * The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.The lesions are confined to the epithelial layer of crypts and lack invasion through the basement membrane into the lamina propria. <br /> * As there are no lymphatic vessels in the lamina propria, lesions with high grade dysplasia are not associated with metastasis.<br /> * High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more &quot;open&quot; appearing nuclei with increasingly prominent nucleoli. <br /> * Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> * Cribriform and crowding, back-to-back glands indicate high-grade dysplasia and are important architectural features to aid in differentiating cases of low vs. high-grade &lt;ref name=&quot;pmid30348703&quot;&gt;{{cite journal| author=Rubio CA| title=Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas. | journal=In Vivo | year= 2018 | volume= 32 | issue= 6 | pages= 1473-1475 | pmid=30348703 | doi=10.21873/invivo.11401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30348703 }} &lt;/ref&gt;.<br /> * The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes&lt;ref name=&quot;pmid15386327&quot;&gt;{{cite journal| author=Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D et al.| title=Interobserver variability in the pathological assessment of malignant colorectal polyps. | journal=Br J Surg | year= 2004 | volume= 91 | issue= 11 | pages= 1479-84 | pmid=15386327 | doi=10.1002/bjs.4588 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15386327 }} &lt;/ref&gt;. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The K-''ras'' oncogene, inactivation of tumor suppressor genes, the ''APC'' gene, on 5q, have important roles in adenoma formation. <br /> * On gross pathology, characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot; /&gt;<br /> **Polypoid or sessile mass<br /> **Cauliflower-like in appearance\<br /> * On microscopic histopathological analysis, characteristic findings of villous adenoma include&lt;ref name=&quot;pmid30063919&quot;&gt;{{cite journal| author=Goverde A, Wagner A, Bruno MJ, Hofstra RMW, Doukas M, van der Weiden MM et al.| title=Routine Molecular Analysis for Lynch Syndrome Among Adenomas or Colorectal Cancer Within a National Screening Program. | journal=Gastroenterology | year= 2018 | volume= 155 | issue= 5 | pages= 1410-1415 | pmid=30063919 | doi=10.1053/j.gastro.2018.07.029 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30063919 }} &lt;/ref&gt;:<br /> **Nuclear changes at the surface of the [[mucosa]]<br /> **Cigar-shaped (elongated) [[nucleus]] (length:width &gt; 3:1) with nuclear [[hyperchromicity|hyperchromasia]]<br /> **Large round [[nuclei]]<br /> **Nuclear crowding<br /> **Positive [[Ki-67]]<br /> * Villous adenomas may cause secretory diarrhea characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis. Increased numbers of goblet cells and increased prostaglandin E2 are responsible for the diarrhea. <br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include&lt;ref name=&quot;pmid30370516&quot;&gt;{{cite journal| author=Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X et al.| title=[Risk analysis of the canceration of colorectal large polyps]. | journal=Zhonghua Wei Chang Wai Ke Za Zhi | year= 2018 | volume= 21 | issue= 10 | pages= 1161-1166 | pmid=30370516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30370516 }} &lt;/ref&gt;:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546107 2019-02-06T03:31:45Z

<p>Jogeet singh sekhon: /* Pathophysiology */</p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Villous adenoma may be classified into 3 subtypes according to histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance.<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;&lt;ref name=&quot;pmid29262150&quot;&gt;{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume= | issue= | pages= | pmid=29262150 | doi= | pmc= | url= }} &lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma.<br /> * The cytological features of low-grade dysplasia include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.<br /> * Pleomorphism and atypical mitoses are absent in low grade dysplasia.<br /> * The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.<br /> * High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more &quot;open&quot; appearing nuclei with increasingly prominent nucleoli. <br /> * Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> * Cribriform and crowding, back-to-back glands indicate high-grade dysplasia and are important architectural features to aid in differentiating cases of low vs. high-grade dysplasia.<br /> * The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The K-''ras'' oncogene, inactivation of tumor suppressor genes, the ''APC'' gene, on 5q, have important roles in adenoma formation. <br /> * On gross pathology, characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot; /&gt;<br /> **Polypoid or sessile mass<br /> **Cauliflower-like in appearance\<br /> * On microscopic histopathological analysis, characteristic findings of villous adenoma include:<br /> **Nuclear changes at the surface of the [[mucosa]]<br /> **Cigar-shaped (elongated) [[nucleus]] (length:width &gt; 3:1) with nuclear [[hyperchromicity|hyperchromasia]]<br /> **Large round [[nuclei]]<br /> **Nuclear crowding<br /> **Positive [[Ki-67]]<br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Villous_adenoma&diff=1546106 2019-02-06T03:29:29Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{SI}} <br /> {{CMG}}; {{AE}} {{MV}}<br /> <br /> {{SK}} Adenomatous polyps; VA; TVA<br /> <br /> ==Overview==<br /> <br /> '''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[gastrointestinal tract]]; it occurs most commonly in the [[colon]]. Villous adenoma may result in [[malignant]] ([[cancerous]]) transformation. Villous adenoma was first discovered by Helwig in 1946. According to the World Health Organization, villous adenoma may be classified into tubular, tubulovillous, and villous (most common) subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignant transformation among villous adenomas is between 15% and 25%. Genes associated with the development of villous adenoma include [[APC]], [[TP53]], [[KRAS|K-ras]], and BAT-26. The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as [[Turcot syndrome|Turcot syndrome]], [[Juvenile polyposis syndrome|juvenile polyposis syndrome]], and [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of [[familial adenomatous polyposis]]. Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> <br /> ==Historical Perspective==<br /> Villous adenoma was first discovered by Helwig in 1946.&lt;ref name=&quot;:0&quot;&gt;Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95&lt;/ref&gt;<br /> <br /> ==Classification==<br /> Villous adenoma may be classified into 3 subtypes according to histological appearance:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *Tubular<br /> *Tubulovillous<br /> *Villous <br /> Villous adenoma can be classified into 4 types according to the gross appearance.<br /> * Flat<br /> * Sessile<br /> * Pedunculated<br /> * Depressed<br /> <br /> ==Pathophysiology==<br /> ===Pathogenesis===<br /> * The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> * Dysplastic changes are present in the adenomas.<br /> * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma.<br /> * The cytological features of low-grade dysplasia include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.<br /> * Pleomorphism and atypical mitoses are absent in low grade dysplasia.<br /> * The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms.<br /> * High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more &quot;open&quot; appearing nuclei with increasingly prominent nucleoli. <br /> * Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. <br /> * Cribriform and crowding, back-to-back glands indicate high-grade dysplasia and are important architectural features to aid in differentiating cases of low vs. high-grade dysplasia.<br /> * The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes. <br /> * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.<br /> * The K-''ras'' oncogene, inactivation of tumor suppressor genes, the ''APC'' gene, on 5q, have important roles in adenoma formation. <br /> * On gross pathology, characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot; /&gt;<br /> **Polypoid or sessile mass<br /> **Cauliflower-like in appearance\<br /> * On microscopic histopathological analysis, characteristic findings of villous adenoma include:<br /> **Nuclear changes at the surface of the [[mucosa]]<br /> **Cigar-shaped (elongated) [[nucleus]] (length:width &gt; 3:1) with nuclear [[hyperchromicity|hyperchromasia]]<br /> **Large round [[nuclei]]<br /> **Nuclear crowding<br /> **Positive [[Ki-67]]<br /> <br /> ==Causes==<br /> Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].<br /> <br /> ==Differentiating Villous Adenoma from Other Diseases==<br /> Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:<br /> * [[Colorectal cancer]]<br /> * Inflammatory fibroid polyp<br /> <br /> ==Epidemiology and Demographics==<br /> ===Prevalence===<br /> The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The [[prevalence]] of adenomas increases with age. <br /> ===Age===<br /> Patients of all age groups may develop villous adenoma.<br /> ===Gender===<br /> Males are more commonly affected with villous adenoma than females. <br /> ===Race===<br /> Villous adenoma more commonly affects caucasians.<br /> <br /> ==Risk Factors==<br /> Common risk factors in the development of villous adenoma include:<br /> * [[Familial adenomatous polyposis]]<br /> * [[Peutz–Jeghers syndrome]]<br /> * [[Turcot syndrome]]<br /> * [[Juvenile polyposis syndrome]]<br /> * [[Cowden disease]]<br /> * [[Bannayan–Riley–Ruvalcaba syndrome]] (Bannayan-Zonana syndrome)<br /> * [[Gardner's syndrome]]<br /> <br /> == Natural History, Complications and Prognosis==<br /> ===Natural History===<br /> The majority of patients with villous adenoma remain asymptomatic for years. Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]]. If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> ===Complications===<br /> Common complications of villous adenoma include:<br /> *[[Bleeding]]<br /> *Obstruction<br /> *Bowel torsion<br /> <br /> ===Prognosis===<br /> The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%. Prognosis becomes poorer with malignant transformation of the lesion. The estimated risk of malignant transformation of villous adenoma is from 15% to 20%.<br /> <br /> == Diagnosis ==<br /> <br /> === Symptoms ===<br /> Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:<br /> *[[Flatulence]]<br /> *[[Abdominal pain]]<br /> *[[Constipation]]<br /> *[[Diarrhea]]<br /> *[[Cramping]]<br /> *Pencil-thin stools<br /> <br /> === Physical Examination ===<br /> Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:<br /> *Bright red blood on digital rectal examination<br /> *Rectal mass<br /> <br /> <br /> === Laboratory Findings ===<br /> There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate positive fecal [[occult blood test]] or [[hypokalemia]].&lt;ref name=&quot;wiki&quot;&gt;Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 &lt;/ref&gt;<br /> <br /> ===Other diagnostic studies===<br /> [[Colonoscopy]] is the diagnostic modality of choice for villous adenoma. On [[colonoscopy]], characteristic findings of villous adenoma include:&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> *A sessile polyp<br /> *Size can range from 0.5 cm to 5 cm <br /> Alternative imaging studies include: <br /> *CT colonography<br /> *Video [[capsule endoscopy]] (less specific)<br /> <br /> == Treatment ==<br /> === Medical Therapy ===<br /> There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.<br /> <br /> === Surgery ===<br /> Surgical removal is the mainstay of therapy for villous adenoma. [[Colonoscopy]] is both diagnostic and therapeutic. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to both the diagnosis and treatment of villous adenoma.&lt;ref name=&quot;pmid19764676&quot;&gt;{{cite journal |vauthors=Osifo OD, Akhiwu W, Efobi CA |title=Small intestinal tubulovillous adenoma--case report and literature review |journal=Niger J Clin Pract |volume=12 |issue=2 |pages=205–7 |year=2009 |pmid=19764676 |doi= |url=}}&lt;/ref&gt;<br /> <br /> === Prevention ===<br /> ====Primary Prevention====<br /> Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of [[familial adenomatous polyposis]]. <br /> ====Secondary Prevention====<br /> Secondary prevention strategies include annual [[occult blood test]] and colonoscopy every ten years for patients above the age of 50.<br /> ==References==<br /> {{Reflist|2}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Gastroenterology]]<br /> [[Category:Surgery]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1542620 2019-01-28T21:49:05Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{JSS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> Hepatosplenic t cell lymphoma is a rare type of non Hodgkins lymphoma that occurs in states of immunosupression such as post organ transplant and treatment of inflammatory bowel disease. Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.'' It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma. The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow. The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year. If left untreated, patients can develop liver failure, pancytopenia or spleen rupture. Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma. Chemotherapy including CHOP is the mainstay of the treatment alongwith bone marrow transplant and radiation therapy.<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a [[T-cell lymphoma classification|peripheral T-cell lymphoma]], a type of [[Non-Hodgkin lymphoma|non Hodgkin's lymphoma]]&lt;ref name=&quot;pmid28516671&quot;&gt;{{cite journal| author=Armitage JO| title=The aggressive peripheral T-cell lymphomas: 2017. | journal=Am J Hematol | year= 2017 | volume= 92 | issue= 7 | pages= 706-715 | pmid=28516671 | doi=10.1002/ajh.24791 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=28516671 }} &lt;/ref&gt;.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma&lt;ref name=&quot;pmid30656034&quot;&gt;{{cite journal| author=Brandt PH, Rahmat LT, Ali SS| title=A rare case of hepatosplenic gamma-delta T-cell lymphoma and secondary hemophagocytic lymphohistiocytosis. | journal=Clin Case Rep | year= 2019 | volume= 7 | issue= 1 | pages= 164-169 | pmid=30656034 | doi=10.1002/ccr3.1924 | pmc=6333078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30656034 }} &lt;/ref&gt;.<br /> * It usually occurs in young men with history of [[immunosuppression]] including solid [[Organ transplant|organ transplantation]]&lt;ref name=&quot;pmid29933321&quot;&gt;{{cite journal| author=Choi Y, Jeon SY, Yoo WH| title=Hepatosplenic T-Cell Lymphoma Arising in a Patient Treated With Tumor Necrosis Factor-α Inhibitors for Ankylosing Spondylitis. | journal=J Clin Rheumatol | year= 2018 | volume= | issue= | pages= | pmid=29933321 | doi=10.1097/RHU.0000000000000805 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29933321 }} &lt;/ref&gt;.<br /> * Patients with [[inflammatory bowel disease]] receiving [[immunosuppressants]] and [[Tumor necrosis factor-alpha|anti-tumor necrosis factor-α]] agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the [[Innate intelligence|innate]] immune system&lt;ref name=&quot;pmid30596219&quot;&gt;{{cite journal| author=Gowda L, Foss F| title=Hepatosplenic T-Cell Lymphomas. | journal=Cancer Treat Res | year= 2019 | volume= 176 | issue= | pages= 185-193 | pmid=30596219 | doi=10.1007/978-3-319-99716-2_9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30596219 }} &lt;/ref&gt;&lt;ref name=&quot;pmid1698028&quot;&gt;{{cite journal| author=Gaulard P, Bourquelot P, Kanavaros P, Haioun C, Le Couedic JP, Divine M et al.| title=Expression of the alpha/beta and gamma/delta T-cell receptors in 57 cases of peripheral T-cell lymphomas. Identification of a subset of gamma/delta T-cell lymphomas. | journal=Am J Pathol | year= 1990 | volume= 137 | issue= 3 | pages= 617-28 | pmid=1698028 | doi= | pmc=1877506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=1698028 }} &lt;/ref&gt;.<br /> * Gamma delta T cells represent the first line of defense against [[Bacteria|bacterial]] [[Peptide|peptides]], such as [[Heat shock protein|heat-shock proteins]].<br /> * Gamma delta T cells are [[CD4]] and [[CD8]] negative, but CD56 positive which is [[NK cell marker]].<br /> * Gamma delta cells respond to a stimuli and are responsible for [[lymphokine]] production and proliferation.<br /> * Gamma delta cells are predominantly located in the [[spleen]], [[liver]] sinusoids and [[Intestine|intestinal]] epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the development of the [[lymphoma]].<br /> * [[Isochromosome]] of the long arm of [[chromosome 7]] is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with [[trisomy]] 8 and a loss of a [[sex chromosome]].<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the [[red pulp]] with small-to-medium-sized [[atypical lymphocytes]]. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the [[white pulp]].<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in [[pancytopenia]].<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as [[hepatosplenomegaly]] without peripheral [[lymphadenopathy]].<br /> * [[Pancytopenia]] and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are&lt;ref name=&quot;pmid29337025&quot;&gt;{{cite journal| author=Yabe M, Miranda RN, Medeiros LJ| title=Hepatosplenic T-cell Lymphoma: a review of clinicopathologic features, pathogenesis, and prognostic factors. | journal=Hum Pathol | year= 2018 | volume= 74 | issue= | pages= 5-16 | pmid=29337025 | doi=10.1016/j.humpath.2018.01.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29337025 }} &lt;/ref&gt;&lt;ref name=&quot;pmid14645001&quot;&gt;{{cite journal| author=Gallamini A, Stelitano C, Calvi R, Bellei M, Mattei D, Vitolo U et al.| title=Peripheral T-cell lymphoma unspecified (PTCL-U): a new prognostic model from a retrospective multicentric clinical study. | journal=Blood | year= 2004 | volume= 103 | issue= 7 | pages= 2474-9 | pmid=14645001 | doi=10.1182/blood-2003-09-3080 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=14645001 }} &lt;/ref&gt;:<br /> * [[Inflammatory bowel disease]]<br /> * [[Organ transplant]] patients (reciever)<br /> * [[Immunosuppresive drug|Immunosuppressive]] medications<br /> * [[Thiopurine|Thiopurines]]<br /> * [[Infliximab]]<br /> * [[Cyclophosphamide]]<br /> * [[Vincristine sulfate|Vincristine]]<br /> * [[Doxorubicin hydrochloride|Doxorubicin]]<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * [[Autoimmune diseases]]<br /> * Patients on immunosuppresant medications.<br /> * Patients on [[Chemotherapy|chemotherapy.]]<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> <br /> === Natural history ===<br /> * Patients have a history of [[immunosupression]] such as inflammatory bowel disease under treatment or organ transplant&lt;ref name=&quot;pmid19237479&quot;&gt;{{cite journal| author=Falchook GS, Vega F, Dang NH, Samaniego F, Rodriguez MA, Champlin RE et al.| title=Hepatosplenic gamma-delta T-cell lymphoma: clinicopathological features and treatment. | journal=Ann Oncol | year= 2009 | volume= 20 | issue= 6 | pages= 1080-5 | pmid=19237479 | doi=10.1093/annonc/mdn751 | pmc=4092251 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=19237479 }} &lt;/ref&gt;.<br /> * The mean age group is 35 years and most of the patients are males.<br /> * Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no [[Lymphadenopathy|lymphadenopathy.]]<br /> * Patients also present with symptoms of liver, spleen and bone marrow dysfunction.<br /> * If left untreated, patients can develop [[Hepatic failure|liver failure]], [[pancytopenia]] or [[spleen rupture]].<br /> <br /> === Complications ===<br /> * [[Hepatomegaly]]<br /> * [[Hepatic failure]]<br /> * [[Portal vein thrombosis]]<br /> * [[Splenomegaly]]<br /> * [[Splenic infarction]]<br /> * Spleen rupture<br /> * [[Splenic vein thrombosis]]<br /> * [[Anemia]]<br /> * [[Thrombocytopenia]]<br /> * [[Neutropenia]]<br /> * Neurological dysfunction if metastasizes to brain.<br /> * [[Gastrointestinal perforation|Intestinal perforation]]<br /> * [[Intestinal obstruction]]<br /> * <br /> <br /> === Prognosis ===<br /> * The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment&lt;ref name=&quot;pmid26872013&quot;&gt;{{cite journal| author=Yabe M, Medeiros LJ, Tang G, Wang SA, Ahmed S, Nieto Y et al.| title=Prognostic Factors of Hepatosplenic T-cell Lymphoma: Clinicopathologic Study of 28 Cases. | journal=Am J Surg Pathol | year= 2016 | volume= 40 | issue= 5 | pages= 676-88 | pmid=26872013 | doi=10.1097/PAS.0000000000000614 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=26872013 }} &lt;/ref&gt;.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> * Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma&lt;ref name=&quot;pmid8141877&quot;&gt;{{cite journal| author=International Non-Hodgkin's Lymphoma Prognostic Factors Project| title=A predictive model for aggressive non-Hodgkin's lymphoma. | journal=N Engl J Med | year= 1993 | volume= 329 | issue= 14 | pages= 987-94 | pmid=8141877 | doi=10.1056/NEJM199309303291402 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=8141877 }} &lt;/ref&gt;.<br /> * CT scan and PET scan are used to assess the spread of the lymphoma.<br /> <br /> === Symptoms ===<br /> The most common symtoms are&lt;ref name=&quot;pmid12419753&quot;&gt;{{cite journal| author=Saito T, Matsuno Y, Tanosaki R, Watanabe T, Kobayashi Y, Tobinai K| title=Gamma delta T-cell neoplasms: a clinicopathological study of 11 cases. | journal=Ann Oncol | year= 2002 | volume= 13 | issue= 11 | pages= 1792-8 | pmid=12419753 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=12419753 }} &lt;/ref&gt;:<br /> * Fever<br /> * Weight loss<br /> * Night sweats<br /> * Pain abdomen<br /> * [[Jaundice]]<br /> * Fatigue<br /> * Recurrent infections<br /> * Bleeding <br /> <br /> ===Physical Examination===<br /> <br /> === Temperature ===<br /> * [[Fever]] is often present<br /> <br /> === Skin ===<br /> * [[Rash]]<br /> <br /> === Thorax ===<br /> * [[Pleural effusion]]<br /> * Chest tenderness<br /> <br /> === Abdomen ===<br /> * [[Splenomegaly]]<br /> * [[Hepatomegaly]]<br /> * [[Ascites]]<br /> * Abdomen tenderness<br /> <br /> === Extremities ===<br /> * Bone tenderness<br /> <br /> ===Laboratory Findings===<br /> * Biopsy of the tumor:<br /> ** [[Histology]] - small-to intermediate sized T lymphocytes infiltrate the sinusoids of the liver and the splenic red pulp.<br /> ** [[Flow cytometry]] and [[immunophenotyping]] - The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression&lt;ref name=&quot;pmid9496260&quot;&gt;{{cite journal| author=Boulland ML, Kanavaros P, Wechsler J, Casiraghi O, Gaulard P| title=Cytotoxic protein expression in natural killer cell lymphomas and in alpha beta and gamma delta peripheral T-cell lymphomas. | journal=J Pathol | year= 1997 | volume= 183 | issue= 4 | pages= 432-9 | pmid=9496260 | doi=10.1002/(SICI)1096-9896(199712)183:4&lt;432::AID-PATH942&gt;3.0.CO;2-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9496260 }} &lt;/ref&gt;.<br /> ** [[Karyotype|Karyotyping]] - Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome&lt;ref name=&quot;pmid8751461&quot;&gt;{{cite journal| author=Jonveaux P, Daniel MT, Martel V, Maarek O, Berger R| title=Isochromosome 7q and trisomy 8 are consistent primary, non-random chromosomal abnormalities associated with hepatosplenic T gamma/delta lymphoma. | journal=Leukemia | year= 1996 | volume= 10 | issue= 9 | pages= 1453-5 | pmid=8751461 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=8751461 }} &lt;/ref&gt;.<br /> * Bone marrow biopsy; The bone marrow is characterized by [[Cancer|neoplastic]] cells in the sinusoids.<br /> * Complete blood count; [[Pancytopenia]]<br /> * Liver function tests: Deranged [[Liver function tests|LFT]]<br /> ** Elevated [[Transaminase|transaminases]]<br /> ** [[Jaundice|Hyperbilirubinemia]]<br /> ** [[Hypoproteinemia]]<br /> ** Elevated [[alkaline phosphatase]] <br /> ** Elevated PT/[[Prothrombin time|INR]]<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with hepatosplenic t cell lymphoma.<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with hepatosplenic t cell lymphoma but [[pleural effusion]] might be present.<br /> <br /> ===Echocardiography or Ultrasound===<br /> * There are no echocardiography findings associated with hepatosplenic t cell lymphoma.<br /> * On ultrasound of abdomen:<br /> ** [[Hepatomegaly]]<br /> ** [[Splenomegaly]]<br /> <br /> ===CT scan===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===MRI===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===Other Imaging Findings===<br /> PET scan: On PET scan, tumor mass can be seen in liver or spleen or if it has metastatsized to any other organ.<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> * [[Induction (biology)|Induction]] therapy&lt;ref name=&quot;pmid20738307&quot;&gt;{{cite journal| author=Simon A, Peoch M, Casassus P, Deconinck E, Colombat P, Desablens B et al.| title=Upfront VIP-reinforced-ABVD (VIP-rABVD) is not superior to CHOP/21 in newly diagnosed peripheral T cell lymphoma. Results of the randomized phase III trial GOELAMS-LTP95. | journal=Br J Haematol | year= 2010 | volume= 151 | issue= 2 | pages= 159-66 | pmid=20738307 | doi=10.1111/j.1365-2141.2010.08329.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=20738307 }} &lt;/ref&gt;<br /> ** [[Cyclophosphamide]]<br /> ** [[Vincristine sulfate|Vincristine]]<br /> ** [[Doxorubicin hydrochloride|Doxorubicin]]<br /> ** [[Prednisolone]]<br /> * [[Consolidation (medicine)|Consolidation]] therapy<br /> ** [[Radiation therapy]]<br /> ** Allogenic [[Hematopoietic stem cell transplantation|bone marrow transplant]]&lt;ref name=&quot;pmid28222648&quot;&gt;{{cite journal| author=Han X, Zhang W, Zhou D, Ruan J, Duan M, Zhu T et al.| title=Autologous stem cell transplantation as frontline strategy for peripheral T-cell lymphoma: A single-centre experience. | journal=J Int Med Res | year= 2017 | volume= 45 | issue= 1 | pages= 290-302 | pmid=28222648 | doi=10.1177/0300060516676725 | pmc=5536587 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=28222648 }} &lt;/ref&gt;<br /> ** Autologous [[Hematopoietic stem cell transplantation|bone marrow transplant]]<br /> * Additional medications given during chemotherapy<br /> ** [[Acyclovir]]<br /> ** [[Fluconazole]]<br /> ** [[Sulfamethoxazole-Trimethoprim|TMP/sulphamethaxozole]]<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of hepaosplenic t cell lymphoma.<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of hepatosplenic t cell lymphoma.<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of hepatosplenic t cell lymphoma.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1542605 2019-01-28T21:16:39Z

<p>Jogeet singh sekhon: /* Treatment */</p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> Hepatosplenic t cell lymphoma is a rare type of non Hodgkins lymphoma that occurs in states of immunosupression such as post organ transplant and treatment of inflammatory bowel disease. Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.'' It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma. The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow. The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year. If left untreated, patients can develop liver failure, pancytopenia or spleen rupture. Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma. Chemotherapy including CHOP is the mainstay of the treatment alongwith bone marrow transplant and radiation therapy.<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a [[T-cell lymphoma classification|peripheral T-cell lymphoma]], a type of [[Non-Hodgkin lymphoma|non Hodgkin's lymphoma]]&lt;ref name=&quot;pmid28516671&quot;&gt;{{cite journal| author=Armitage JO| title=The aggressive peripheral T-cell lymphomas: 2017. | journal=Am J Hematol | year= 2017 | volume= 92 | issue= 7 | pages= 706-715 | pmid=28516671 | doi=10.1002/ajh.24791 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=28516671 }} &lt;/ref&gt;.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma&lt;ref name=&quot;pmid30656034&quot;&gt;{{cite journal| author=Brandt PH, Rahmat LT, Ali SS| title=A rare case of hepatosplenic gamma-delta T-cell lymphoma and secondary hemophagocytic lymphohistiocytosis. | journal=Clin Case Rep | year= 2019 | volume= 7 | issue= 1 | pages= 164-169 | pmid=30656034 | doi=10.1002/ccr3.1924 | pmc=6333078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30656034 }} &lt;/ref&gt;.<br /> * It usually occurs in young men with history of [[immunosuppression]] including solid [[Organ transplant|organ transplantation]]&lt;ref name=&quot;pmid29933321&quot;&gt;{{cite journal| author=Choi Y, Jeon SY, Yoo WH| title=Hepatosplenic T-Cell Lymphoma Arising in a Patient Treated With Tumor Necrosis Factor-α Inhibitors for Ankylosing Spondylitis. | journal=J Clin Rheumatol | year= 2018 | volume= | issue= | pages= | pmid=29933321 | doi=10.1097/RHU.0000000000000805 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29933321 }} &lt;/ref&gt;.<br /> * Patients with [[inflammatory bowel disease]] receiving [[immunosuppressants]] and [[Tumor necrosis factor-alpha|anti-tumor necrosis factor-α]] agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the [[Innate intelligence|innate]] immune system&lt;ref name=&quot;pmid30596219&quot;&gt;{{cite journal| author=Gowda L, Foss F| title=Hepatosplenic T-Cell Lymphomas. | journal=Cancer Treat Res | year= 2019 | volume= 176 | issue= | pages= 185-193 | pmid=30596219 | doi=10.1007/978-3-319-99716-2_9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30596219 }} &lt;/ref&gt;&lt;ref name=&quot;pmid1698028&quot;&gt;{{cite journal| author=Gaulard P, Bourquelot P, Kanavaros P, Haioun C, Le Couedic JP, Divine M et al.| title=Expression of the alpha/beta and gamma/delta T-cell receptors in 57 cases of peripheral T-cell lymphomas. Identification of a subset of gamma/delta T-cell lymphomas. | journal=Am J Pathol | year= 1990 | volume= 137 | issue= 3 | pages= 617-28 | pmid=1698028 | doi= | pmc=1877506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=1698028 }} &lt;/ref&gt;.<br /> * Gamma delta T cells represent the first line of defense against [[Bacteria|bacterial]] [[Peptide|peptides]], such as [[Heat shock protein|heat-shock proteins]].<br /> * Gamma delta T cells are [[CD4]] and [[CD8]] negative, but CD56 positive which is [[NK cell marker]].<br /> * Gamma delta cells respond to a stimuli and are responsible for [[lymphokine]] production and proliferation.<br /> * Gamma delta cells are predominantly located in the [[spleen]], [[liver]] sinusoids and [[Intestine|intestinal]] epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the development of the [[lymphoma]].<br /> * [[Isochromosome]] of the long arm of [[chromosome 7]] is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with [[trisomy]] 8 and a loss of a [[sex chromosome]].<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the [[red pulp]] with small-to-medium-sized [[atypical lymphocytes]]. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the [[white pulp]].<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in [[pancytopenia]].<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as [[hepatosplenomegaly]] without peripheral [[lymphadenopathy]].<br /> * [[Pancytopenia]] and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are&lt;ref name=&quot;pmid29337025&quot;&gt;{{cite journal| author=Yabe M, Miranda RN, Medeiros LJ| title=Hepatosplenic T-cell Lymphoma: a review of clinicopathologic features, pathogenesis, and prognostic factors. | journal=Hum Pathol | year= 2018 | volume= 74 | issue= | pages= 5-16 | pmid=29337025 | doi=10.1016/j.humpath.2018.01.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29337025 }} &lt;/ref&gt;:<br /> * [[Inflammatory bowel disease]]<br /> * [[Organ transplant]] patients (reciever)<br /> * [[Immunosuppresive drug|Immunosuppressive]] medications<br /> * [[Thiopurine|Thiopurines]]<br /> * [[Infliximab]]<br /> * [[Cyclophosphamide]]<br /> * [[Vincristine sulfate|Vincristine]]<br /> * [[Doxorubicin hydrochloride|Doxorubicin]]<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * [[Autoimmune diseases]]<br /> * Patients on immunosuppresant medications.<br /> * Patients on [[Chemotherapy|chemotherapy.]]<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> <br /> === Natural history ===<br /> * Patients have a history of [[immunosupression]] such as inflammatory bowel disease under treatment or organ transplant&lt;ref name=&quot;pmid19237479&quot;&gt;{{cite journal| author=Falchook GS, Vega F, Dang NH, Samaniego F, Rodriguez MA, Champlin RE et al.| title=Hepatosplenic gamma-delta T-cell lymphoma: clinicopathological features and treatment. | journal=Ann Oncol | year= 2009 | volume= 20 | issue= 6 | pages= 1080-5 | pmid=19237479 | doi=10.1093/annonc/mdn751 | pmc=4092251 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=19237479 }} &lt;/ref&gt;.<br /> * The mean age group is 35 years and most of the patients are males.<br /> * Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no [[Lymphadenopathy|lymphadenopathy.]]<br /> * Patients also present with symptoms of liver, spleen and bone marrow dysfunction.<br /> * If left untreated, patients can develop [[Hepatic failure|liver failure]], [[pancytopenia]] or [[spleen rupture]].<br /> <br /> === Complications ===<br /> * [[Hepatomegaly]]<br /> * [[Hepatic failure]]<br /> * [[Portal vein thrombosis]]<br /> * [[Splenomegaly]]<br /> * [[Splenic infarction]]<br /> * Spleen rupture<br /> * [[Splenic vein thrombosis]]<br /> * [[Anemia]]<br /> * [[Thrombocytopenia]]<br /> * [[Neutropenia]]<br /> * Neurological dysfunction if metastasizes to brain.<br /> * [[Gastrointestinal perforation|Intestinal perforation]]<br /> * [[Intestinal obstruction]]<br /> * <br /> <br /> === Prognosis ===<br /> * The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment&lt;ref name=&quot;pmid26872013&quot;&gt;{{cite journal| author=Yabe M, Medeiros LJ, Tang G, Wang SA, Ahmed S, Nieto Y et al.| title=Prognostic Factors of Hepatosplenic T-cell Lymphoma: Clinicopathologic Study of 28 Cases. | journal=Am J Surg Pathol | year= 2016 | volume= 40 | issue= 5 | pages= 676-88 | pmid=26872013 | doi=10.1097/PAS.0000000000000614 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=26872013 }} &lt;/ref&gt;.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> * Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma.<br /> * CT scan and PET scan are used to assess the spread of the lymphoma.<br /> <br /> === Symptoms ===<br /> * Fever<br /> * Weight loss<br /> * Night sweats<br /> * Pain abdomen<br /> * [[Jaundice]]<br /> * Fatigue<br /> * Recurrent infections<br /> * Bleeding <br /> <br /> ===Physical Examination===<br /> <br /> === Temperature ===<br /> * [[Fever]] is often present<br /> <br /> === Skin ===<br /> * [[Rash]]<br /> <br /> === Thorax ===<br /> * [[Pleural effusion]]<br /> * Chest tenderness<br /> <br /> === Abdomen ===<br /> * [[Splenomegaly]]<br /> * [[Hepatomegaly]]<br /> * [[Ascites]]<br /> * Abdomen tenderness<br /> <br /> === Extremities ===<br /> * Bone tenderness<br /> <br /> ===Laboratory Findings===<br /> * Biopsy of the tumor:<br /> ** [[Histology]] - small-to intermediate sized T lymphocytes infiltrate the sinusoids of the liver and the splenic red pulp.<br /> ** [[Flow cytometry]] and [[immunophenotyping]] - The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> ** [[Karyotype|Karyotyping]] - Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Bone marrow biopsy; The bone marrow is characterized by [[Cancer|neoplastic]] cells in the sinusoids.<br /> * Complete blood count; [[Pancytopenia]]<br /> * Liver function tests: Deranged [[Liver function tests|LFT]]<br /> ** Elevated [[Transaminase|transaminases]]<br /> ** [[Jaundice|Hyperbilirubinemia]]<br /> ** [[Hypoproteinemia]]<br /> ** Elevated [[alkaline phosphatase]] <br /> ** Elevated PT/[[Prothrombin time|INR]]<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with hepatosplenic t cell lymphoma.<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with hepatosplenic t cell lymphoma but [[pleural effusion]] might be present.<br /> <br /> ===Echocardiography or Ultrasound===<br /> * There are no echocardiography findings associated with hepatosplenic t cell lymphoma.<br /> * On ultrasound of abdomen:<br /> ** [[Hepatomegaly]]<br /> ** [[Splenomegaly]]<br /> <br /> ===CT scan===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===MRI===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===Other Imaging Findings===<br /> PET scan: On PET scan, tumor mass can be seen in liver or spleen or if it has metastatsized to any other organ.<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> * [[Induction (biology)|Induction]] therapy<br /> ** [[Cyclophosphamide]]<br /> ** [[Vincristine sulfate|Vincristine]]<br /> ** [[Doxorubicin hydrochloride|Doxorubicin]]<br /> ** [[Prednisolone]]<br /> * [[Consolidation (medicine)|Consolidation]] therapy<br /> ** [[Radiation therapy]]<br /> ** Allogenic [[Hematopoietic stem cell transplantation|bone marrow transplant]]<br /> ** Autologous [[Hematopoietic stem cell transplantation|bone marrow transplant]]<br /> * Additional medications given during chemotherapy<br /> ** [[Acyclovir]]<br /> ** [[Fluconazole]]<br /> ** [[Sulfamethoxazole-Trimethoprim|TMP/sulphamethaxozole]]<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of hepaosplenic t cell lymphoma.<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of hepatosplenic t cell lymphoma.<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of hepatosplenic t cell lymphoma.<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1539426 2019-01-23T05:12:31Z

<p>Jogeet singh sekhon: /* Physical Examination */</p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma&lt;ref name=&quot;pmid28516671&quot;&gt;{{cite journal| author=Armitage JO| title=The aggressive peripheral T-cell lymphomas: 2017. | journal=Am J Hematol | year= 2017 | volume= 92 | issue= 7 | pages= 706-715 | pmid=28516671 | doi=10.1002/ajh.24791 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=28516671 }} &lt;/ref&gt;.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma&lt;ref name=&quot;pmid30656034&quot;&gt;{{cite journal| author=Brandt PH, Rahmat LT, Ali SS| title=A rare case of hepatosplenic gamma-delta T-cell lymphoma and secondary hemophagocytic lymphohistiocytosis. | journal=Clin Case Rep | year= 2019 | volume= 7 | issue= 1 | pages= 164-169 | pmid=30656034 | doi=10.1002/ccr3.1924 | pmc=6333078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30656034 }} &lt;/ref&gt;.<br /> * It usually occurs in young men with history of immunosuppression including solid organ transplantation and leukemia&lt;ref name=&quot;pmid29933321&quot;&gt;{{cite journal| author=Choi Y, Jeon SY, Yoo WH| title=Hepatosplenic T-Cell Lymphoma Arising in a Patient Treated With Tumor Necrosis Factor-α Inhibitors for Ankylosing Spondylitis. | journal=J Clin Rheumatol | year= 2018 | volume= | issue= | pages= | pmid=29933321 | doi=10.1097/RHU.0000000000000805 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29933321 }} &lt;/ref&gt;.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the innate immune system&lt;ref name=&quot;pmid30596219&quot;&gt;{{cite journal| author=Gowda L, Foss F| title=Hepatosplenic T-Cell Lymphomas. | journal=Cancer Treat Res | year= 2019 | volume= 176 | issue= | pages= 185-193 | pmid=30596219 | doi=10.1007/978-3-319-99716-2_9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30596219 }} &lt;/ref&gt;&lt;ref name=&quot;pmid1698028&quot;&gt;{{cite journal| author=Gaulard P, Bourquelot P, Kanavaros P, Haioun C, Le Couedic JP, Divine M et al.| title=Expression of the alpha/beta and gamma/delta T-cell receptors in 57 cases of peripheral T-cell lymphomas. Identification of a subset of gamma/delta T-cell lymphomas. | journal=Am J Pathol | year= 1990 | volume= 137 | issue= 3 | pages= 617-28 | pmid=1698028 | doi= | pmc=1877506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=1698028 }} &lt;/ref&gt;.<br /> * Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.<br /> * Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> * Pancytopenia and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are&lt;ref name=&quot;pmid29337025&quot;&gt;{{cite journal| author=Yabe M, Miranda RN, Medeiros LJ| title=Hepatosplenic T-cell Lymphoma: a review of clinicopathologic features, pathogenesis, and prognostic factors. | journal=Hum Pathol | year= 2018 | volume= 74 | issue= | pages= 5-16 | pmid=29337025 | doi=10.1016/j.humpath.2018.01.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29337025 }} &lt;/ref&gt;:<br /> * Inflammatory bowel disease<br /> * Organ transplant patients (reciever)<br /> * Immunosuppresent medications<br /> * Thiopurines<br /> * Infliximab<br /> * Cyclophosphamide<br /> * Vincristine<br /> * Doxorubicin<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * Immunodeficiency diseases.<br /> * Patients on immunosuppresant medications.<br /> * Patients on chemotherapy.<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> <br /> === Natural history ===<br /> * Patients have a history of immunosupression such as inflammatory bowel disease under treatment or organ transplant&lt;ref name=&quot;pmid19237479&quot;&gt;{{cite journal| author=Falchook GS, Vega F, Dang NH, Samaniego F, Rodriguez MA, Champlin RE et al.| title=Hepatosplenic gamma-delta T-cell lymphoma: clinicopathological features and treatment. | journal=Ann Oncol | year= 2009 | volume= 20 | issue= 6 | pages= 1080-5 | pmid=19237479 | doi=10.1093/annonc/mdn751 | pmc=4092251 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=19237479 }} &lt;/ref&gt;.<br /> * The mean age group is 35 years and most of the patients are males.<br /> * Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no lymphadenopathy.<br /> * Patients also present with symptoms of liver, spleen and bone marrow dysfunction.<br /> * If left untreated, patients can develop liver failure, pancytopenia or spleen rupture.<br /> <br /> === Complications ===<br /> * Hepatomegaly<br /> * Hepatic failure<br /> * Portal vein thrombosis<br /> * Splenomegaly<br /> * Splenic infarction<br /> * Spleen rupture<br /> * Splenic vein thrombosis<br /> * Anemia<br /> * Thrombocytopenia<br /> * Neutropenia<br /> * Neurological dysfunction if metastasizes to brain.<br /> * Intestinal perforation<br /> * Intestinal obstruction<br /> * <br /> <br /> === Prognosis ===<br /> * The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment&lt;ref name=&quot;pmid26872013&quot;&gt;{{cite journal| author=Yabe M, Medeiros LJ, Tang G, Wang SA, Ahmed S, Nieto Y et al.| title=Prognostic Factors of Hepatosplenic T-cell Lymphoma: Clinicopathologic Study of 28 Cases. | journal=Am J Surg Pathol | year= 2016 | volume= 40 | issue= 5 | pages= 676-88 | pmid=26872013 | doi=10.1097/PAS.0000000000000614 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=26872013 }} &lt;/ref&gt;.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> * Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma.<br /> * CT scan and PET scan are used to assess the spread of the lymphoma.<br /> <br /> === Symptoms ===<br /> * Fever<br /> * Weight loss<br /> * Night sweats<br /> * Pain abdomen<br /> * Jaundice<br /> * Fatigue<br /> * Recurrent infections<br /> * Bleeding <br /> <br /> ===Physical Examination===<br /> <br /> === Temperature ===<br /> * [[Fever]] is often present<br /> <br /> === Skin ===<br /> * [[Rash]]<br /> <br /> === Thorax ===<br /> * [[Pleural effusion]]<br /> * Chest tenderness<br /> <br /> === Abdomen ===<br /> * [[Splenomegaly]]<br /> * [[Hepatomegaly]]<br /> * [[Ascites]]<br /> * Abdomen tenderness<br /> <br /> === Extremities ===<br /> * Bone tenderness<br /> <br /> ===Laboratory Findings===<br /> * Biopsy of the tumor:<br /> ** Histology - small-to intermediate sized T lymphocytes infiltrate the sinusoids of the liver and the splenic red pulp.<br /> ** Flow cytometry and immunophenotyping - The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> ** Karyotyping - Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Bone marrow biopsy; The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Complete blood count; Pancytopenia<br /> * Liver function tests: Deranged LFT<br /> ** Elevated transaminases<br /> ** Hyperbilirubinemia<br /> ** Hypoproteinemia<br /> ** Elevated [[alkaline phosphatase]] <br /> ** Elevated PT/INR<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with hepatosplenic t cell lymphoma.<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with hepatosplenic t cell lymphoma but pleural effusion might be present.<br /> <br /> ===Echocardiography or Ultrasound===<br /> * There are no echocardiography findings associated with hepatosplenic t cell lymphoma.<br /> * On ultrasound of abdomen:<br /> ** Hepatomegaly<br /> ** Splenomegaly<br /> <br /> ===CT scan===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===MRI===<br /> Tumor mass can be seen in liver or spleen or both.<br /> <br /> ===Other Imaging Findings===<br /> PET scan: On PET scan, tumor mass can be seen in liver or spleen or if it has metastatsized to any other organ.<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1538407 2019-01-21T23:14:13Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma&lt;ref name=&quot;pmid28516671&quot;&gt;{{cite journal| author=Armitage JO| title=The aggressive peripheral T-cell lymphomas: 2017. | journal=Am J Hematol | year= 2017 | volume= 92 | issue= 7 | pages= 706-715 | pmid=28516671 | doi=10.1002/ajh.24791 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=28516671 }} &lt;/ref&gt;.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma&lt;ref name=&quot;pmid30656034&quot;&gt;{{cite journal| author=Brandt PH, Rahmat LT, Ali SS| title=A rare case of hepatosplenic gamma-delta T-cell lymphoma and secondary hemophagocytic lymphohistiocytosis. | journal=Clin Case Rep | year= 2019 | volume= 7 | issue= 1 | pages= 164-169 | pmid=30656034 | doi=10.1002/ccr3.1924 | pmc=6333078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30656034 }} &lt;/ref&gt;.<br /> * It usually occurs in young men with history of immunosuppression including solid organ transplantation and leukemia&lt;ref name=&quot;pmid29933321&quot;&gt;{{cite journal| author=Choi Y, Jeon SY, Yoo WH| title=Hepatosplenic T-Cell Lymphoma Arising in a Patient Treated With Tumor Necrosis Factor-α Inhibitors for Ankylosing Spondylitis. | journal=J Clin Rheumatol | year= 2018 | volume= | issue= | pages= | pmid=29933321 | doi=10.1097/RHU.0000000000000805 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29933321 }} &lt;/ref&gt;.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the innate immune system&lt;ref name=&quot;pmid30596219&quot;&gt;{{cite journal| author=Gowda L, Foss F| title=Hepatosplenic T-Cell Lymphomas. | journal=Cancer Treat Res | year= 2019 | volume= 176 | issue= | pages= 185-193 | pmid=30596219 | doi=10.1007/978-3-319-99716-2_9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=30596219 }} &lt;/ref&gt;&lt;ref name=&quot;pmid1698028&quot;&gt;{{cite journal| author=Gaulard P, Bourquelot P, Kanavaros P, Haioun C, Le Couedic JP, Divine M et al.| title=Expression of the alpha/beta and gamma/delta T-cell receptors in 57 cases of peripheral T-cell lymphomas. Identification of a subset of gamma/delta T-cell lymphomas. | journal=Am J Pathol | year= 1990 | volume= 137 | issue= 3 | pages= 617-28 | pmid=1698028 | doi= | pmc=1877506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=1698028 }} &lt;/ref&gt;.<br /> * Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.<br /> * Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> * Pancytopenia and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are&lt;ref name=&quot;pmid29337025&quot;&gt;{{cite journal| author=Yabe M, Miranda RN, Medeiros LJ| title=Hepatosplenic T-cell Lymphoma: a review of clinicopathologic features, pathogenesis, and prognostic factors. | journal=Hum Pathol | year= 2018 | volume= 74 | issue= | pages= 5-16 | pmid=29337025 | doi=10.1016/j.humpath.2018.01.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29337025 }} &lt;/ref&gt;:<br /> * Inflammatory bowel disease<br /> * Organ transplant patients (reciever)<br /> * Immunosuppresent medications<br /> * Thiopurines<br /> * Infliximab<br /> * Cyclophosphamide<br /> * Vincristine<br /> * Doxorubicin<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * Immunodeficiency diseases.<br /> * Patients on immunosuppresant medications.<br /> * Patients on chemotherapy.<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> <br /> === Natural history ===<br /> * Patients have a history of immunosupression such as inflammatory bowel disease under treatment or organ transplant&lt;ref name=&quot;pmid19237479&quot;&gt;{{cite journal| author=Falchook GS, Vega F, Dang NH, Samaniego F, Rodriguez MA, Champlin RE et al.| title=Hepatosplenic gamma-delta T-cell lymphoma: clinicopathological features and treatment. | journal=Ann Oncol | year= 2009 | volume= 20 | issue= 6 | pages= 1080-5 | pmid=19237479 | doi=10.1093/annonc/mdn751 | pmc=4092251 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=19237479 }} &lt;/ref&gt;.<br /> * The mean age group is 35 years and most of the patients are males.<br /> * Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no lymphadenopathy.<br /> * Patients also present with symptoms of liver, spleen and bone marrow dysfunction.<br /> * If left untreated, patients can develop liver failure, pancytopenia or spleen rupture.<br /> <br /> === Complications ===<br /> * Hepatomegaly<br /> * Hepatic failure<br /> * Portal vein thrombosis<br /> * Splenomegaly<br /> * Splenic infarction<br /> * Spleen rupture<br /> * Splenic vein thrombosis<br /> * Anemia<br /> * Thrombocytopenia<br /> * Neutropenia<br /> * Neurological dysfunction if metastasizes to brain.<br /> * Intestinal perforation<br /> * Intestinal obstruction<br /> * <br /> <br /> === Prognosis ===<br /> * The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment&lt;ref name=&quot;pmid26872013&quot;&gt;{{cite journal| author=Yabe M, Medeiros LJ, Tang G, Wang SA, Ahmed S, Nieto Y et al.| title=Prognostic Factors of Hepatosplenic T-cell Lymphoma: Clinicopathologic Study of 28 Cases. | journal=Am J Surg Pathol | year= 2016 | volume= 40 | issue= 5 | pages= 676-88 | pmid=26872013 | doi=10.1097/PAS.0000000000000614 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=26872013 }} &lt;/ref&gt;.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> * Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma.<br /> * CT scan and PET scan are used to assess the spread of the lymphoma.<br /> <br /> === Symptoms ===<br /> * Fever<br /> * Weight loss<br /> * Night sweats<br /> * Pain abdomen<br /> * Jaundice<br /> * Fatigue<br /> * Recurrent infections<br /> * Bleeding <br /> <br /> ===Physical Examination===<br /> Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is highly suggestive of [disease name].<br /> <br /> ===Laboratory Findings===<br /> An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].<br /> <br /> OR<br /> <br /> [Test] is usually normal among patients with [disease name].<br /> <br /> OR<br /> <br /> Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].<br /> <br /> OR<br /> <br /> There are no diagnostic laboratory findings associated with [disease name].<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with [disease name].<br /> <br /> OR<br /> <br /> An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with [disease name].<br /> <br /> OR<br /> <br /> An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Echocardiography or Ultrasound===<br /> There are no echocardiography/ultrasound findings associated with [disease name].<br /> <br /> OR<br /> <br /> Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===CT scan===<br /> There are no CT scan findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===MRI===<br /> There are no MRI findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Other Imaging Findings===<br /> There are no other imaging findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===Other Diagnostic Studies===<br /> There are no other diagnostic studies associated with [disease name].<br /> <br /> OR<br /> <br /> [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1538402 2019-01-21T23:05:35Z

<p>Jogeet singh sekhon: /* Natural History, Complications, and Prognosis */</p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma.<br /> * It usually occurs in young men with history of immunosuppression including solid organ transplantation and leukemia.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the innate immune system.<br /> * Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.<br /> * Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> * Pancytopenia and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are:<br /> * Inflammatory bowel disease<br /> * Organ transplant patients (reciever)<br /> * Immunosuppresent medications<br /> * Thiopurines<br /> * Infliximab<br /> * Cyclophosphamide<br /> * Vincristine<br /> * Doxorubicin<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * Immunodeficiency diseases.<br /> * Patients on immunosuppresant medications.<br /> * Patients on chemotherapy.<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> <br /> === Natural history ===<br /> * Patients have a history of immunosupression such as inflammatory bowel disease under treatment or organ transplant.<br /> * The mean age group is 35 years and most of the patients are males.<br /> * Initial symptoms are fever, weight loss, night sweats and then progress to more severe symptoms depending on the organ involvement but there is no lymphadenopathy.<br /> * Patients also present with symptoms of liver, spleen and bone marrow dysfunction.<br /> * If left untreated, patients can develop liver failure, pancytopenia or spleen rupture.<br /> <br /> === Complications ===<br /> * Hepatomegaly<br /> * Hepatic failure<br /> * Portal vein thrombosis<br /> * Splenomegaly<br /> * Splenic infarction<br /> * Spleen rupture<br /> * Splenic vein thrombosis<br /> * Anemia<br /> * Thrombocytopenia<br /> * Neutropenia<br /> * Neurological dysfunction if metastasizes to brain.<br /> * Intestinal perforation<br /> * Intestinal obstruction<br /> * <br /> <br /> === Prognosis ===<br /> * The prognosis is very poor, with patients dying within 2-3 years of diagnosis even after recieving treatment.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> * Biopsy of the tumor is the gold standard diagnostic test for diagnosing hepatosplenic t cell lymphoma.<br /> * CT scan and PET scan are used to assess the spread of the lymphoma.<br /> <br /> === Symptoms ===<br /> * Fever<br /> * Weight loss<br /> * Night sweats<br /> * Pain abdomen<br /> * Jaundice<br /> * Fatigue<br /> * Recurrent infections<br /> * Bleeding <br /> <br /> ===Physical Examination===<br /> Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is highly suggestive of [disease name].<br /> <br /> ===Laboratory Findings===<br /> An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].<br /> <br /> OR<br /> <br /> [Test] is usually normal among patients with [disease name].<br /> <br /> OR<br /> <br /> Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].<br /> <br /> OR<br /> <br /> There are no diagnostic laboratory findings associated with [disease name].<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with [disease name].<br /> <br /> OR<br /> <br /> An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with [disease name].<br /> <br /> OR<br /> <br /> An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Echocardiography or Ultrasound===<br /> There are no echocardiography/ultrasound findings associated with [disease name].<br /> <br /> OR<br /> <br /> Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===CT scan===<br /> There are no CT scan findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===MRI===<br /> There are no MRI findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Other Imaging Findings===<br /> There are no other imaging findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===Other Diagnostic Studies===<br /> There are no other diagnostic studies associated with [disease name].<br /> <br /> OR<br /> <br /> [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1537845 2019-01-21T02:19:30Z

<p>Jogeet singh sekhon: /* Classification */</p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> Hepatosplenic T cell lymphoma was discovered by Farcet ''et al in 1990.''<br /> <br /> ==Classification==<br /> There is no established system for the classification of hepatosplenic t cell lymphoma.<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma.<br /> * It usually occurs in young men with history of immunosuppression including solid organ transplantation and leukemia.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the innate immune system.<br /> * Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.<br /> * Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> * Pancytopenia and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Common causes of hepatosplenic t cell lymphoma are:<br /> * Inflammatory bowel disease<br /> * Organ transplant patients (reciever)<br /> * Immunosuppresent medications<br /> * Thiopurines<br /> * Infliximab<br /> * Cyclophosphamide<br /> * Vincristine<br /> * Doxorubicin<br /> <br /> ==Differentiating hepatosplenic t cell lymphoma from Other Diseases==<br /> <br /> ==Epidemiology and Demographics==<br /> * The incidence of hepatosplenic t cell lymphoma is 0.3 per 100000 individuals per year.<br /> * It occurs in younger group of patients, most cases falling in 20-40 years of age group.<br /> * Men are more affected than the females.<br /> <br /> ==Risk Factors==<br /> Common risk factors include:<br /> * Immunodeficiency diseases.<br /> * Patients on immunosuppresant medications.<br /> * Patients on chemotherapy.<br /> * Inflammatory bowel disease<br /> * Organ transplant patients.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for hepatosplenic t cell lymphoma.<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].<br /> <br /> OR<br /> <br /> Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].<br /> <br /> OR<br /> <br /> Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> laboratory findings include pancytopaenia and abnormal liver chemistry with elevated alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase.<br /> <br /> The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> There are no established criteria for the diagnosis of [disease name].<br /> <br /> ===History and Symptoms===<br /> The majority of patients with [disease name] are asymptomatic.<br /> <br /> OR<br /> <br /> The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].<br /> <br /> ===Physical Examination===<br /> Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is highly suggestive of [disease name].<br /> <br /> ===Laboratory Findings===<br /> An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].<br /> <br /> OR<br /> <br /> [Test] is usually normal among patients with [disease name].<br /> <br /> OR<br /> <br /> Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].<br /> <br /> OR<br /> <br /> There are no diagnostic laboratory findings associated with [disease name].<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with [disease name].<br /> <br /> OR<br /> <br /> An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with [disease name].<br /> <br /> OR<br /> <br /> An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Echocardiography or Ultrasound===<br /> There are no echocardiography/ultrasound findings associated with [disease name].<br /> <br /> OR<br /> <br /> Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===CT scan===<br /> There are no CT scan findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===MRI===<br /> There are no MRI findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Other Imaging Findings===<br /> There are no other imaging findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===Other Diagnostic Studies===<br /> There are no other diagnostic studies associated with [disease name].<br /> <br /> OR<br /> <br /> [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1537817 2019-01-21T00:51:30Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> [Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].<br /> <br /> The association between [important risk factor/cause] and [disease name] was made in/during [year/event].<br /> <br /> In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].<br /> <br /> In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].<br /> <br /> There have been several outbreaks of [disease name], including -----.<br /> <br /> In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].<br /> <br /> ==Classification==<br /> There is no established system for the classification of [disease name].<br /> <br /> OR<br /> <br /> [Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].<br /> <br /> OR<br /> <br /> [Disease name] may be classified into [large number &gt; 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3].<br /> [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].<br /> <br /> OR<br /> <br /> Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.<br /> <br /> OR<br /> <br /> If the staging system involves specific and characteristic findings and features:<br /> According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].<br /> <br /> OR<br /> <br /> The staging of [malignancy name] is based on the [staging system].<br /> <br /> OR<br /> <br /> There is no established system for the staging of [malignancy name].<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a peripheral T-cell lymphoma, a type of non Hodgkin's lymphoma.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma.<br /> * It usually occurs in young men with history of immunosuppression including solid organ transplantation and leukemia.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing hepatosplenic T-cell lymphoma. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface which are a part of the innate immune system.<br /> * Gamma delta T cells represent the first line of defense against bacterial peptides, such as heat-shock proteins.<br /> * Gamma delta T cells are CD4 and CD8 negative, but CD56 positive which is NK cell marker.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen, liver sinusoids and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * Isochromosome of the long arm of chromosome 7 is a genetic abnormality described in hepatosplenic t cell lymphoma. It could also be in association with trisomy 8 and a loss of a sex chromosome.<br /> * Mutations in ''SETD2, INO80, TET3'' and ''STAT5B'' occur exclusively in hepatosplenic t cell lymphoma as compared to other T and B cell lymphoma types.<br /> * The lymphoma is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> * Pancytopenia and abnormal liver functions are the laboratory findings.<br /> * Histology and immunohistochemistry of the tumor biopsy shows portal and sinusoidal infiltration by atypical small-to-medium sized lymphocytes with hyperchromatic nuclei and low mitotic activity.<br /> <br /> ==Causes==<br /> Disease name] may be caused by [cause1], [cause2], or [cause3].<br /> <br /> OR<br /> <br /> Common causes of [disease] include [cause1], [cause2], and [cause3].<br /> <br /> OR<br /> <br /> The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].<br /> <br /> OR<br /> <br /> The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click [[Pericarditis causes#Overview|here]].<br /> <br /> ==Differentiating ((Page name)) from Other Diseases==<br /> [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].<br /> <br /> OR<br /> <br /> [Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].<br /> <br /> ==Epidemiology and Demographics==<br /> The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.<br /> <br /> OR<br /> <br /> In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.<br /> <br /> OR<br /> <br /> In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.<br /> <br /> <br /> <br /> Patients of all age groups may develop [disease name].<br /> <br /> OR<br /> <br /> The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.<br /> <br /> OR<br /> <br /> [Disease name] commonly affects individuals younger than/older than [number of years] years of age.<br /> <br /> OR <br /> <br /> [Chronic disease name] is usually first diagnosed among [age group].<br /> <br /> OR<br /> <br /> [Acute disease name] commonly affects [age group].<br /> <br /> <br /> <br /> There is no racial predilection to [disease name].<br /> <br /> OR<br /> <br /> [Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].<br /> <br /> <br /> <br /> [Disease name] affects men and women equally.<br /> <br /> OR<br /> <br /> [Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number &gt; 1] to 1.<br /> <br /> <br /> <br /> The majority of [disease name] cases are reported in [geographical region].<br /> <br /> OR<br /> <br /> [Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].<br /> <br /> ==Risk Factors==<br /> There are no established risk factors for [disease name].<br /> <br /> OR<br /> <br /> The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].<br /> <br /> OR<br /> <br /> Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].<br /> <br /> OR<br /> <br /> Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for [disease/malignancy].<br /> <br /> OR<br /> <br /> According to the [guideline name], screening for [disease name] is not recommended.<br /> <br /> OR<br /> <br /> According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].<br /> <br /> OR<br /> <br /> Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].<br /> <br /> OR<br /> <br /> Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> laboratory findings include pancytopaenia and abnormal liver chemistry with elevated alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase.<br /> <br /> The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> There are no established criteria for the diagnosis of [disease name].<br /> <br /> ===History and Symptoms===<br /> The majority of patients with [disease name] are asymptomatic.<br /> <br /> OR<br /> <br /> The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].<br /> <br /> ===Physical Examination===<br /> Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is highly suggestive of [disease name].<br /> <br /> ===Laboratory Findings===<br /> An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].<br /> <br /> OR<br /> <br /> [Test] is usually normal among patients with [disease name].<br /> <br /> OR<br /> <br /> Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].<br /> <br /> OR<br /> <br /> There are no diagnostic laboratory findings associated with [disease name].<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with [disease name].<br /> <br /> OR<br /> <br /> An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with [disease name].<br /> <br /> OR<br /> <br /> An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Echocardiography or Ultrasound===<br /> There are no echocardiography/ultrasound findings associated with [disease name].<br /> <br /> OR<br /> <br /> Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===CT scan===<br /> There are no CT scan findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===MRI===<br /> There are no MRI findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Other Imaging Findings===<br /> There are no other imaging findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===Other Diagnostic Studies===<br /> There are no other diagnostic studies associated with [disease name].<br /> <br /> OR<br /> <br /> [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Hepatosplenic_T_cell_lymphoma&diff=1512938 2018-12-31T12:28:16Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> <br /> '''For patient information, click [[Hepatosplenic T cell lymphoma (patient information)|here]]'''<br /> {{Hepatosplenic T cell lymphoma}}<br /> * {{CMG}}; {{AE}} {{AS}}<br /> '''''Synonyms and Keywords:''''' Hepatosplenic γδ T-cell lymphoma, Hepatosplenic gamma delta T-cell lymphoma, HSTCL<br /> <br /> {{SK}} <br /> <br /> ==Overview==<br /> <br /> ==Historical Perspective==<br /> [Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].<br /> <br /> The association between [important risk factor/cause] and [disease name] was made in/during [year/event].<br /> <br /> In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].<br /> <br /> In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].<br /> <br /> There have been several outbreaks of [disease name], including -----.<br /> <br /> In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].<br /> <br /> ==Classification==<br /> There is no established system for the classification of [disease name].<br /> <br /> OR<br /> <br /> [Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].<br /> <br /> OR<br /> <br /> [Disease name] may be classified into [large number &gt; 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3].<br /> [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].<br /> <br /> OR<br /> <br /> Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.<br /> <br /> OR<br /> <br /> If the staging system involves specific and characteristic findings and features:<br /> According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].<br /> <br /> OR<br /> <br /> The staging of [malignancy name] is based on the [staging system].<br /> <br /> OR<br /> <br /> There is no established system for the staging of [malignancy name].<br /> <br /> ==Pathophysiology==<br /> * Hepatosplenic T-cell lymphoma is a type of peripheral T-cell lymphoma.<br /> * It is also known as ‘gamma-delta hepatosplenic T-cell lymphoma.<br /> * It occurrs in young men with history of immunosuppression including solid organ transplantation and leukemia.<br /> * Patients with inflammatory bowel diseases receiving immunosuppressants and anti-tumor necrosis factor-α agent are also at risk for developing HSTCL. <br /> * The T-cell receptor consists of either a gamma delta or aplha beta entity on their cell surface.<br /> * Gamma delta cells respond to a stimuli and are responsible for lymphokine production and proliferation.<br /> * Gamma delta cells are predominantly located in the spleen and intestinal epithelium.<br /> * 75 % of the cases are of gamma delta phenotype and the rest are apha beta phenotype.<br /> * Chronic antigen stimulation in states of immunosuppression is responsible for the deveopment of the lymphoma.<br /> * It is characterized by malignant T-cell proliferation in the sinusoids of the liver, sinuses and red pulp of the spleen, and sinuses of the bone marrow.<br /> * Splenic involvement is characterized by diffuse involvement of the red pulp with small-to-medium-sized atypical lymphocytes. <br /> * The atypical lymphocytes are present within the cords and sinuses of the red pulp.<br /> * There occurs a complete loss of the white pulp.<br /> * The liver also shows sinusoidal infiltration by neoplastic lymphoid cells. <br /> * The bone marrow is characterized by neoplastic cells in the sinusoids.<br /> * Bone marrow infiltration results in pancytopenia.<br /> * The lymphoma cells are typically CD2+, CD3+, CD4−, CD5−, CD7+, CD8− CD42+, CD52+, CD76+, CD82+ with either gamma-delta or alpha-beta T-cell phenotypic receptor expression.<br /> * It manifests as hepatosplenomegaly without peripheral lymphadenopathy.<br /> <br /> ==Causes==<br /> Disease name] may be caused by [cause1], [cause2], or [cause3].<br /> <br /> OR<br /> <br /> Common causes of [disease] include [cause1], [cause2], and [cause3].<br /> <br /> OR<br /> <br /> The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].<br /> <br /> OR<br /> <br /> The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click [[Pericarditis causes#Overview|here]].<br /> <br /> ==Differentiating ((Page name)) from Other Diseases==<br /> [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].<br /> <br /> OR<br /> <br /> [Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].<br /> <br /> ==Epidemiology and Demographics==<br /> The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.<br /> <br /> OR<br /> <br /> In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.<br /> <br /> OR<br /> <br /> In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.<br /> <br /> <br /> <br /> Patients of all age groups may develop [disease name].<br /> <br /> OR<br /> <br /> The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.<br /> <br /> OR<br /> <br /> [Disease name] commonly affects individuals younger than/older than [number of years] years of age.<br /> <br /> OR <br /> <br /> [Chronic disease name] is usually first diagnosed among [age group].<br /> <br /> OR<br /> <br /> [Acute disease name] commonly affects [age group].<br /> <br /> <br /> <br /> There is no racial predilection to [disease name].<br /> <br /> OR<br /> <br /> [Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].<br /> <br /> <br /> <br /> [Disease name] affects men and women equally.<br /> <br /> OR<br /> <br /> [Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number &gt; 1] to 1.<br /> <br /> <br /> <br /> The majority of [disease name] cases are reported in [geographical region].<br /> <br /> OR<br /> <br /> [Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].<br /> <br /> ==Risk Factors==<br /> There are no established risk factors for [disease name].<br /> <br /> OR<br /> <br /> The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].<br /> <br /> OR<br /> <br /> Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].<br /> <br /> OR<br /> <br /> Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.<br /> <br /> ==Screening==<br /> There is insufficient evidence to recommend routine screening for [disease/malignancy].<br /> <br /> OR<br /> <br /> According to the [guideline name], screening for [disease name] is not recommended.<br /> <br /> OR<br /> <br /> According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].<br /> <br /> ==Natural History, Complications, and Prognosis==<br /> If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].<br /> <br /> OR<br /> <br /> Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].<br /> <br /> OR<br /> <br /> Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.<br /> <br /> ==Diagnosis==<br /> ===Diagnostic Study of Choice===<br /> The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].<br /> <br /> OR<br /> <br /> There are no established criteria for the diagnosis of [disease name].<br /> <br /> ===History and Symptoms===<br /> The majority of patients with [disease name] are asymptomatic.<br /> <br /> OR<br /> <br /> The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].<br /> <br /> ===Physical Examination===<br /> Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> The presence of [finding(s)] on physical examination is highly suggestive of [disease name].<br /> <br /> ===Laboratory Findings===<br /> An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].<br /> <br /> OR<br /> <br /> Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].<br /> <br /> OR<br /> <br /> [Test] is usually normal among patients with [disease name].<br /> <br /> OR<br /> <br /> Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].<br /> <br /> OR<br /> <br /> There are no diagnostic laboratory findings associated with [disease name].<br /> <br /> ===Electrocardiogram===<br /> There are no ECG findings associated with [disease name].<br /> <br /> OR<br /> <br /> An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===X-ray===<br /> There are no x-ray findings associated with [disease name].<br /> <br /> OR<br /> <br /> An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Echocardiography or Ultrasound===<br /> There are no echocardiography/ultrasound findings associated with [disease name].<br /> <br /> OR<br /> <br /> Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===CT scan===<br /> There are no CT scan findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===MRI===<br /> There are no MRI findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].<br /> <br /> ===Other Imaging Findings===<br /> There are no other imaging findings associated with [disease name].<br /> <br /> OR<br /> <br /> [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> ===Other Diagnostic Studies===<br /> There are no other diagnostic studies associated with [disease name].<br /> <br /> OR<br /> <br /> [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].<br /> <br /> OR<br /> <br /> Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].<br /> <br /> ==Treatment==<br /> ===Medical Therapy===<br /> There is no treatment for [disease name]; the mainstay of therapy is supportive care.<br /> <br /> OR<br /> <br /> Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].<br /> <br /> OR<br /> <br /> The majority of cases of [disease name] are self-limited and require only supportive care.<br /> <br /> OR<br /> <br /> [Disease name] is a medical emergency and requires prompt treatment.<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is [therapy].<br /> <br /> OR<br />  <br /> The optimal therapy for [malignancy name] depends on the stage at diagnosis.<br /> <br /> OR<br /> <br /> [Therapy] is recommended among all patients who develop [disease name].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].<br /> <br /> OR<br /> <br /> Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].<br /> <br /> OR<br /> <br /> Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].<br /> <br /> OR<br /> <br /> Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].<br /> <br /> ===Surgery===<br /> Surgical intervention is not recommended for the management of [disease name].<br /> <br /> OR<br /> <br /> Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]<br /> <br /> OR<br /> <br /> The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].<br /> <br /> OR<br /> <br /> The feasibility of surgery depends on the stage of [malignancy] at diagnosis.<br /> <br /> OR<br /> <br /> Surgery is the mainstay of treatment for [disease or malignancy].<br /> <br /> ===Primary Prevention===<br /> There are no established measures for the primary prevention of [disease name].<br /> <br /> OR<br /> <br /> There are no available vaccines against [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].<br /> <br /> OR<br /> <br /> [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ===Secondary Prevention===<br /> There are no established measures for the secondary prevention of [disease name].<br /> <br /> OR<br /> <br /> Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].<br /> <br /> ==References==<br /> {{reflist|2}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma&diff=1512542 2018-12-28T01:25:37Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> '''For patient information click [[{{PAGENAME}} (patient information)|here]]'''<br /> <br /> {{CMG}}; {{AE}} {{AS}} {{JSS}}<br /> <br /> {{SK}} FL; Centroblastic and centrocytic lymphoma; Brill-Symmers Disease.<br /> <br /> ==[[Follicular lymphoma overview|Overview]]==<br /> <br /> ==[[Follicular lymphoma historical perspective|Historical Perspective]]==<br /> <br /> ==[[Follicular lymphoma classification|Classification]]==<br /> <br /> ==[[Follicular lymphoma pathophysiology|Pathophysiology]]==<br /> <br /> ==[[Follicular lymphoma causes|Causes]]==<br /> <br /> ==[[Follicular lymphoma differential diagnosis|Differentiating Follicular lymphoma from other Diseases]]==<br /> <br /> ==[[Follicular lymphoma epidemiology and demographics|Epidemiology and Demographics]]==<br /> <br /> ==[[Follicular lymphoma risk factors|Risk Factors]]==<br /> <br /> ==[[Follicular lymphoma screening|Screening]]==<br /> <br /> ==[[Follicular lymphoma natural history, complications and prognosis|Natural History, Complications and Prognosis]]==<br /> <br /> ==Diagnosis==<br /> [[Follicular lymphoma staging|Staging]] | [[Follicular lymphoma history and symptoms|History and Symptoms]] | [[Follicular lymphoma physical examination|Physical Examination]] | [[Follicular lymphoma laboratory findings|Laboratory Findings]] | [[Follicular lymphoma chest x ray|Chest X Ray]] | [[Follicular lymphoma CT|CT]] | [[Follicular lymphoma MRI|MRI]] | [[Follicular lymphoma ultrasound|Ultrasound]] | [[Follicular lymphoma biopsy|Biopsy]] | [[Follicular lymphoma other imaging findings|Other Imaging Findings]] | [[Follicular lymphoma other diagnostic studies|Other Diagnostic Studies]]<br /> <br /> ==Treatment==<br /> [[Follicular lymphoma medical therapy|Medical Therapy]] | [[Follicular lymphoma surgery|Surgery]] | [[Follicular lymphoma cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Follicular lymphoma future or investigational therapies|Future or Investigational Therapies]]<br /> <br /> ==Case Studies==<br /> [[Follicular lymphoma case study one|Case #1]]<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Oncology]]<br /> {{Hematological malignancy histology}}<br /> <br /> {{WikiDoc Help Menu}}<br /> {{WikiDoc Sources}}<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_historical_perspective&diff=1512541 2018-12-28T01:23:22Z

<p>Jogeet singh sekhon: /* References */</p> <hr /> <div>__NOTOC__<br /> <br /> == Overview ==<br /> Follicular lymphoma was described in 1925 by Brill and Symmers.<br /> <br /> == Historical perspective ==<br /> * Follicular lymphoma was first described in 1925 by Brill and Symmers&lt;ref name=&quot;pmid17325883&quot;&gt;{{cite journal| author=van Besien K, Schouten H| title=Follicular lymphoma: a historical overview. | journal=Leuk Lymphoma | year= 2007 | volume= 48 | issue= 2 | pages= 232-43 | pmid=17325883 | doi=10.1080/10428190601059746 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=17325883 }} &lt;/ref&gt;.<br /> * It was earlier known as Brill – Symmers disease after the authors of the original papers.<br /> * Most of its clinical features were described by the early 1940s<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Needs content]]<br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_medical_therapy&diff=1512540 2018-12-28T01:17:54Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}} {{AE}} {{AS}}<br /> ==Overview==<br /> The optimal therapy for follicular lymphoma depends on the stage at diagnosis, age, and prognostic scores. The predominant therapy for follicular lymphoma is [[chemotherapy]]. Adjunctive hematopoietic [[stem cell transplantation]] and [[radioimmunotherapy]] may be required.<br /> ==Medical Therapy==<br /> * The treatment of follicular lymphoma is based on the stage of the disease&lt;ref name=&quot;pmid23777769&quot;&gt;{{cite journal| author=Tan D, Horning SJ, Hoppe RT, Levy R, Rosenberg SA, Sigal BM et al.| title=Improvements in observed and relative survival in follicular grade 1-2 lymphoma during 4 decades: the Stanford University experience. | journal=Blood | year= 2013 | volume= 122 | issue= 6 | pages= 981-7 | pmid=23777769 | doi=10.1182/blood-2013-03-491514 | pmc=3739040 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23777769 }} &lt;/ref&gt;&lt;ref name=&quot;pmid22211428&quot;&gt;{{cite journal| author=McNamara C, Davies J, Dyer M, Hoskin P, Illidge T, Lyttelton M et al.| title=Guidelines on the investigation and management of follicular lymphoma. | journal=Br J Haematol | year= 2012 | volume= 156 | issue= 4 | pages= 446-67 | pmid=22211428 | doi=10.1111/j.1365-2141.2011.08969.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22211428 }} &lt;/ref&gt;&lt;ref name=&quot;pmid24602760&quot;&gt;{{cite journal| author=Ardeshna KM, Qian W, Smith P, Braganca N, Lowry L, Patrick P et al.| title=Rituximab versus a watch-and-wait approach in patients with advanced-stage, asymptomatic, non-bulky follicular lymphoma: an open-label randomised phase 3 trial. | journal=Lancet Oncol | year= 2014 | volume= 15 | issue= 4 | pages= 424-35 | pmid=24602760 | doi=10.1016/S1470-2045(14)70027-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=24602760 }} &lt;/ref&gt;&lt;ref name=&quot;pmid27664263&quot;&gt;{{cite journal| author=Dreyling M, Ghielmini M, Rule S, Salles G, Vitolo U, Ladetto M et al.| title=Newly diagnosed and relapsed follicular lymphoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. | journal=Ann Oncol | year= 2016 | volume= 27 | issue= suppl 5 | pages= v83-v90 | pmid=27664263 | doi=10.1093/annonc/mdw400 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=27664263 }} &lt;/ref&gt;<br /> .<br /> * For stage 1 and 2, radiotherapy is done.<br /> * For stages 3 and 4, several chemotherapeutic drugs are used for treatment of follicular lymphoma.<br /> * Chemotherapy is started when there is high tumor bulk load which includes the following:<br /> *** A tumor &gt;7 cm in diameter<br /> *** Three nodes in three distinct areas, each &gt;3 cm in diameter<br /> *** Symptomatic spleen enlargement<br /> *** Organ compression<br /> *** Ascites or pleural effusion<br /> <br /> === Follicular lymphoma ===<br /> 1. Stage 1 and 2:<br /> * Radiation doses of 24-30 Gy have been used .<br /> 2. High tumor bulk load<br /> <br /> 2.1. Adult:<br /> #* Preferred regime 1. '''Bendamustine + rituximab - Day 1: Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; IV , Days 1 and 2: Bendamustine 90mg/m&lt;sup&gt;2&lt;/sup&gt; IV over 30–60 minutes.''' '''Repeat every 4 weeks for 6 cycles'''<br /> #* Preferred regime 2. '''Bendamustine + obinutuzumab - Days 1 and 2: Bendamustine 90mg/m&lt;sup&gt;2&lt;/sup&gt; IV''' '''Days 1, 8, 15 of Cycle 1: Obintuzumab 1000mg IV followed by:''' '''Days 1 and 2: Bendamustine 90mg/m&lt;sup&gt;2&lt;/sup&gt; IV''' '''Days 1 of Subsequent Cycles: Obintuzumab 1000mg IV.''' '''Repeat every 4 weeks for 6 cycles.'''<br /> #* Preferred regime 3. '''RCHOP (Category 1) - Day 0: Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; IV''' '''Day 1: Cyclophosphamide 750mg/m&lt;sup&gt;2&lt;/sup&gt; IV + doxorubicin 50mg/m&lt;sup&gt;2&lt;/sup&gt; IV + vincristine 1.4mg/m&lt;sup&gt;2&lt;/sup&gt; IV (max 2mg)''' '''Days 1–5: Prednisone 100mg/m&lt;sup&gt;2&lt;/sup&gt; orally.''' '''Repeat every 3 weeks for 6 to 8 cycles'''<br /> #* Preferred regime 4. '''CHOP + obinutuzumab - Day 1: Cyclophosphamide 750mg/m&lt;sup&gt;2&lt;/sup&gt; IV + doxorubicin 50mg/m&lt;sup&gt;2&lt;/sup&gt; IV + vincristine 1.4mg/m&lt;sup&gt;2&lt;/sup&gt; IV (max 2mg)''' '''Days 1–5: Prednisone 100mg/m&lt;sup&gt;2&lt;/sup&gt; orally''' '''Days 1, 8, 15 of Cycle 1: Obintuzumab 1000mg IV followed by:''' '''Day 1: Cyclophosphamide 750mg/m&lt;sup&gt;2&lt;/sup&gt; IV + doxorubicin 50mg/m&lt;sup&gt;2&lt;/sup&gt; IV + vincristine 1.4mg/m&lt;sup&gt;2&lt;/sup&gt; IV (max 2mg)''' '''Days 1–5: Prednisone 100mg/m&lt;sup&gt;2&lt;/sup&gt; orally''' '''Days 1 of Subsequent Cycles: Obintuzumab 1000mg IV.''' '''Repeat every 3 weeks for 6 to 8 cycles.'''<br /> #* Alternate regime 1. '''CVP + obinutuzumab - Day 1: Cyclophosphamide 750mg/v IV + vincristine 1.4mg/v IV (max 2mg)''' '''Days 1–5: Prednisone 40mg/v orally''' '''Days 1, 8, 15 of Cycle 1: Obintuzumab 1000mg IV followed by:''' '''Day 1: Cyclophosphamide 750mg/v IV + vincristine 1.4mg/v IV (max 2mg)''' '''Days 1–5: Prednisone 40mg/m&lt;sup&gt;2&lt;/sup&gt; orally''' '''Days 1 of Subsequent Cycles: Obintuzumab 1000mg IV.''' '''Repeat every 3 weeks for 6 to 8 cycles'''<br /> #* Alternate regime 2. '''Rituximab, Day 1: Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; IV.''' '''Repeat every 7 days for 4 cycles'''<br /> 2.2. Elderly<br /> * Preferred regime 1. '''Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; IV.''' '''Repeat every 7 days for 4 cycles''' <br /> * Preferred regime 2. '''Single agent alkylator ± rituximab - Chlorambucil 0.1mg/kg/day for 45 days then on days 1–15, monthly for 4 months''' '''• Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; weekly for 4 doses, then monthly for 4 infusions'''<br /> 3. Consolidation and extended dosing<br /> * '''Rituximab maintenance - Day 1: Rituximab 375mg/m&lt;sup&gt;2&lt;/sup&gt; IV.''' '''Repeat every 8 weeks for 12 cycles for patients initially presenting with high tumor burden.'''<br /> * '''Obinutuzumab maintenance - Day 1: Obinutuzumab 1000 mg IV.''' '''Repeat every 8 weeks for 12 cycles.'''<br /> * '''Radioimmunotherapy - 90Yttrium-ibritumomab-tiuxetan 15 MBq/kg (0.4 mCi/kg) single dose after induction with chemotherapy.'''<br /> '''High-dose therapy with autologous stem cell rescue and Allogeneic stem cell transplant for highly selected patients.'''<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_physical_examination&diff=1512513 2018-12-27T23:44:15Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> Common physical examination findings of follicular lymphoma include [[fever]], [[rash]], [[splenomegaly]], [[Lymphadenopathy|peripheral lymphadenopathy]], and [[Lymphadenopathy|central lymphadenopathy]].<br /> ==Physical Examination==<br /> The following physical examination findings may be present among patients with follicular lymphoma&lt;ref name=&quot;pmid9166827&quot;&gt;{{cite journal| author=| title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project. | journal=Blood | year= 1997 | volume= 89 | issue= 11 | pages= 3909-18 | pmid=9166827 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9166827 }} &lt;/ref&gt;&lt;ref name=&quot;pmid11877266&quot;&gt;{{cite journal| author=Lorsbach RB, Shay-Seymore D, Moore J, Banks PM, Hasserjian RP, Sandlund JT et al.| title=Clinicopathologic analysis of follicular lymphoma occurring in children. | journal=Blood | year= 2002 | volume= 99 | issue= 6 | pages= 1959-64 | pmid=11877266 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=11877266 }} &lt;/ref&gt;&lt;ref name=&quot;pmid21375524&quot;&gt;{{cite journal| author=Fernández de Larrea C, Martínez-Pozo A, Mercadal S, García A, Gutierrez-García G, Valera A et al.| title=Initial features and outcome of cutaneous and non-cutaneous primary extranodal follicular lymphoma. | journal=Br J Haematol | year= 2011 | volume= 153 | issue= 3 | pages= 334-40 | pmid=21375524 | doi=10.1111/j.1365-2141.2011.08596.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=21375524 }} &lt;/ref&gt;&lt;ref name=&quot;pmid25176983&quot;&gt;{{cite journal| author=Ganapathi KA, Pittaluga S, Odejide OO, Freedman AS, Jaffe ES| title=Early lymphoid lesions: conceptual, diagnostic and clinical challenges. | journal=Haematologica | year= 2014 | volume= 99 | issue= 9 | pages= 1421-32 | pmid=25176983 | doi=10.3324/haematol.2014.107938 | pmc=4562530 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=25176983 }} &lt;/ref&gt;:<br /> ===Temperature===<br /> * [[Fever]] <br /> ===Skin===<br /> * [[Pruritus]]<br /> * [[Petechiae]] <br /> ===Neck===<br /> * [[Lymphadenopathy|Cervical lymphadenopathy]]<br /> ===Thorax===<br /> * Thoracic masses suggestive of [[Lymphadenopathy|central lymphadenopathy]]<br /> * Chest tenderness<br /> ===Abdomen===<br /> * [[Abdominal mass]]es suggestive of [[Lymphadenopathy|central lymphadenopathy]]<br /> * [[Splenomegaly]] <br /> * [[Hepatomegaly]]<br /> * [[Abdominal tenderness]]<br /> ===Extremities===<br /> * [[Lymphadenopathy|Peripheral lymphadenopathy]]<br /> ===CNS===<br /> * [[Seizures]]<br /> <br /> =====Head=====<br /> &lt;gallery&gt;<br /> Image:Non hodgkin's lymphoma05.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma05.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> &lt;/gallery&gt;<br /> =====Neck=====<br /> &lt;gallery&gt;<br /> Image:Non hodgkin's lymphoma01.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma02.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma03.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma04.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma07.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma08.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma09.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> Image:Non hodgkin's lymphoma10.jpg|:Non hodgkin's lymphoma. &lt;SMALL&gt;&lt;SMALL&gt;''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''&lt;ref name=&quot;Dermatology Atlas&quot;&gt;{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}&lt;/ref&gt;&lt;/SMALL&gt;&lt;/SMALL&gt;<br /> &lt;/gallery&gt;<br /> <br /> ===References===<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_history_and_symptoms&diff=1512507 2018-12-27T23:26:51Z

<p>Jogeet singh sekhon: /* History */</p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> The most common symptoms of follicular lymphoma include [[fever]], [[weight loss]], [[night sweats]], [[skin rash]], painless swelling in the neck,under arm, groin, thorax and abdomen, and chest pain, abdominal pain, and bone pain.<br /> <br /> === History ===<br /> * Peripheral adenopathy in cervical, axillary, inguinal and or femoral regions&lt;ref name=&quot;pmid23023713&quot;&gt;{{cite journal| author=Kridel R, Sehn LH, Gascoyne RD| title=Pathogenesis of follicular lymphoma. | journal=J Clin Invest | year= 2012 | volume= 122 | issue= 10 | pages= 3424-31 | pmid=23023713 | doi=10.1172/JCI63186 | pmc=3461914 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23023713 }} &lt;/ref&gt;&lt;ref name=&quot;pmid9166827&quot;&gt;{{cite journal| author=| title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project. | journal=Blood | year= 1997 | volume= 89 | issue= 11 | pages= 3909-18 | pmid=9166827 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9166827 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7028244&quot;&gt;{{cite journal| author=Winberg CD, Nathwani BN, Bearman RM, Rappaport H| title=Follicular (nodular) lymphoma during the first two decades of life: a clinicopathologic study of 12 patients. | journal=Cancer | year= 1981 | volume= 48 | issue= 10 | pages= 2223-35 | pmid=7028244 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7028244 }} &lt;/ref&gt;&lt;ref name=&quot;pmid21375524&quot;&gt;{{cite journal| author=Fernández de Larrea C, Martínez-Pozo A, Mercadal S, García A, Gutierrez-García G, Valera A et al.| title=Initial features and outcome of cutaneous and non-cutaneous primary extranodal follicular lymphoma. | journal=Br J Haematol | year= 2011 | volume= 153 | issue= 3 | pages= 334-40 | pmid=21375524 | doi=10.1111/j.1365-2141.2011.08596.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=21375524 }} &lt;/ref&gt;<br /> * Weight loss<br /> * Anorexia<br /> * Night sweats<br /> * Unexplained fever<br /> <br /> ===Symptoms===<br /> Symptoms of follicular lymphoma include the following:&lt;ref name=&quot;seer&quot;&gt;National Cancer Institute. Surveillance, Epidemiology, and End Results Program 2015. http://seer.cancer.gov&lt;/ref&gt;<br /> <br /> * [[Fever]]<br /> * [[Weight loss]]<br /> * [[Night sweats]]<br /> * [[Skin rash]]<br /> * [[Chest pain]]<br /> * [[Abdominal pain]]<br /> * [[Bone pain]]<br /> * [[Cough]]<br /> * [[Dyspnea]]<br /> * Painless swelling in the neck, axilla, groin, thorax and abdomen<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_history_and_symptoms&diff=1512504 2018-12-27T23:22:47Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> The most common symptoms of follicular lymphoma include [[fever]], [[weight loss]], [[night sweats]], [[skin rash]], painless swelling in the neck,under arm, groin, thorax and abdomen, and chest pain, abdominal pain, and bone pain.<br /> <br /> === History ===<br /> * Peripheral adenopathy in cervical, axillary, inguinal and or femoral regions&lt;ref name=&quot;pmid23023713&quot;&gt;{{cite journal| author=Kridel R, Sehn LH, Gascoyne RD| title=Pathogenesis of follicular lymphoma. | journal=J Clin Invest | year= 2012 | volume= 122 | issue= 10 | pages= 3424-31 | pmid=23023713 | doi=10.1172/JCI63186 | pmc=3461914 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23023713 }} &lt;/ref&gt;&lt;ref name=&quot;pmid9166827&quot;&gt;{{cite journal| author=| title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project. | journal=Blood | year= 1997 | volume= 89 | issue= 11 | pages= 3909-18 | pmid=9166827 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9166827 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7028244&quot;&gt;{{cite journal| author=Winberg CD, Nathwani BN, Bearman RM, Rappaport H| title=Follicular (nodular) lymphoma during the first two decades of life: a clinicopathologic study of 12 patients. | journal=Cancer | year= 1981 | volume= 48 | issue= 10 | pages= 2223-35 | pmid=7028244 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7028244 }} &lt;/ref&gt;&lt;ref name=&quot;pmid21375524&quot;&gt;{{cite journal| author=Fernández de Larrea C, Martínez-Pozo A, Mercadal S, García A, Gutierrez-García G, Valera A et al.| title=Initial features and outcome of cutaneous and non-cutaneous primary extranodal follicular lymphoma. | journal=Br J Haematol | year= 2011 | volume= 153 | issue= 3 | pages= 334-40 | pmid=21375524 | doi=10.1111/j.1365-2141.2011.08596.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=21375524 }} &lt;/ref&gt;<br /> * Abdominal masses<br /> * Peripheral neuropathies<br /> * Unexplained fever<br /> <br /> ===Symptoms===<br /> Symptoms of follicular lymphoma include the following:&lt;ref name=&quot;seer&quot;&gt;National Cancer Institute. Surveillance, Epidemiology, and End Results Program 2015. http://seer.cancer.gov&lt;/ref&gt;<br /> <br /> * [[Fever]]<br /> * [[Weight loss]]<br /> * [[Night sweats]]<br /> * [[Skin rash]]<br /> * [[Chest pain]]<br /> * [[Abdominal pain]]<br /> * [[Bone pain]]<br /> * [[Cough]]<br /> * [[Dyspnea]]<br /> * Painless swelling in the neck, axilla, groin, thorax and abdomen<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_diagnostic_study_of_choice&diff=1512501 2018-12-27T23:05:01Z

<p>Jogeet singh sekhon: /* Diagnostic Study of Choice */</p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> {{CMG}}; {{AE}}<br /> == Overview ==<br /> Laboratory tests for the diagnosis of follicular lymphoma include [[lymph node biopsy]], [[complete blood count]] (CBC), blood chemistry studies, cytogenetics studies, [[flow cytometry]], [[immunohistochemistry]], [[FISH]], [[genetic testing]], and [[immunophenotyping]]. [[CT]], [[MRI]], and [[PET]] may be helpful in the diagnosis and assessing the spread of follicular lymphoma. Other diagnostic studies for the diagnosis of follicular lymphoma include [[bone marrow aspiration]] and biopsy, [[laparoscopy]], and [[laparotomy]]. <br /> <br /> == Diagnostic Study of Choice ==<br /> * [[Lymph node biopsy]] is the diagnostic study of choice&lt;ref name=&quot;pmid25176983&quot;&gt;{{cite journal| author=Ganapathi KA, Pittaluga S, Odejide OO, Freedman AS, Jaffe ES| title=Early lymphoid lesions: conceptual, diagnostic and clinical challenges. | journal=Haematologica | year= 2014 | volume= 99 | issue= 9 | pages= 1421-32 | pmid=25176983 | doi=10.3324/haematol.2014.107938 | pmc=4562530 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=25176983 }} &lt;/ref&gt;&lt;ref name=&quot;pmid29314206&quot;&gt;{{cite journal| author=Freedman A| title=Follicular lymphoma: 2018 update on diagnosis and management. | journal=Am J Hematol | year= 2018 | volume= 93 | issue= 2 | pages= 296-305 | pmid=29314206 | doi=10.1002/ajh.24937 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=29314206 }} &lt;/ref&gt;&lt;ref name=&quot;pmid23691443&quot;&gt;{{cite journal| author=| title=Guidelines for the diagnosis and treatment of follicular lymphoma in China. | journal=Cancer Biol Med | year= 2013 | volume= 10 | issue= 1 | pages= 36-42 | pmid=23691443 | doi=10.7497/j.issn.2095-3941.2013.01.006 | pmc=3643683 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23691443 }} &lt;/ref&gt;.<br /> * Histopathological, Immunohistochemistry, FISh and cytogenetic studies are conducted on the tissue sample.<br /> * Other diagnostic tests that are done are :<br /> ** [[Complete blood count]] (CBC)<br /> ** Complete metabolic panel<br /> ** [[Hepatitis B virus|HBV]], [[Hepatitis C|HCV]] and [[Human Immunodeficiency Virus (HIV)|HIV]] testing<br /> ** Serum [[Lactate dehydrogenase|LDH]] levels and serum β&lt;sub&gt;2&lt;/sub&gt;-microglobulin levels.<br /> ** [[Bone marrow biopsy]] and aspiration<br /> ** Chest x ray and abdominal ultrasound<br /> ** CT scan<br /> ** PET scan<br /> ** Cytogenetics studies<br /> ** [[Flow cytometry]]<br /> ** [[Immunohistochemistry]]<br /> ** [[FISH]]<br /> ** [[Genetic testing]]<br /> ** [[Immunophenotyping]]: [[BCL-2]]+, BCL6+, [[CD5]]-, CD10+, [[CD19]], [[CD20]], [[CD22]], [[CD43]], [[CD79a]], heavy and light chains rearranged, t(14;18)(q32:q21)-85% with rearrangement of ''[[BCL-2]]'' gene.<br /> ** [[Endoscopy]] for gastrointestinal lymphoma&lt;ref name=&quot;pmid26819532&quot;&gt;{{cite journal| author=Iwamuro M, Kondo E, Takata K, Yoshino T, Okada H| title=Diagnosis of follicular lymphoma of the gastrointestinal tract: A better initial diagnostic workup. | journal=World J Gastroenterol | year= 2016 | volume= 22 | issue= 4 | pages= 1674-83 | pmid=26819532 | doi=10.3748/wjg.v22.i4.1674 | pmc=4721998 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=26819532 }} &lt;/ref&gt;<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> {{WH}}<br /> {{WS}}</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_natural_history,_complications_and_prognosis&diff=1512499 2018-12-27T22:50:29Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> Follicular lymphoma presents in the age group of 60-65 with systemic symptoms of [[fever]], [[weight loss]], [[anorexia]], [[night sweats]] and other organ dependent symptoms based on the [[Metastasis|metastatic]] spread of the lymphoma. Complications arise from the systemic effects of the lymphoma and metastasis. The prognosis is evaluated from follicular lymphoma international prognostic index which divides patients into 3 groups.<br /> <br /> == Natural history ==<br /> * Follicular lymphoma presents in older age group people of age 60-65&lt;ref name=&quot;pmid23023713&quot;&gt;{{cite journal| author=Kridel R, Sehn LH, Gascoyne RD| title=Pathogenesis of follicular lymphoma. | journal=J Clin Invest | year= 2012 | volume= 122 | issue= 10 | pages= 3424-31 | pmid=23023713 | doi=10.1172/JCI63186 | pmc=3461914 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23023713 }} &lt;/ref&gt;&lt;ref name=&quot;pmid9166827&quot;&gt;{{cite journal| author=| title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project. | journal=Blood | year= 1997 | volume= 89 | issue= 11 | pages= 3909-18 | pmid=9166827 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9166827 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7028244&quot;&gt;{{cite journal| author=Winberg CD, Nathwani BN, Bearman RM, Rappaport H| title=Follicular (nodular) lymphoma during the first two decades of life: a clinicopathologic study of 12 patients. | journal=Cancer | year= 1981 | volume= 48 | issue= 10 | pages= 2223-35 | pmid=7028244 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7028244 }} &lt;/ref&gt;&lt;ref name=&quot;pmid21375524&quot;&gt;{{cite journal| author=Fernández de Larrea C, Martínez-Pozo A, Mercadal S, García A, Gutierrez-García G, Valera A et al.| title=Initial features and outcome of cutaneous and non-cutaneous primary extranodal follicular lymphoma. | journal=Br J Haematol | year= 2011 | volume= 153 | issue= 3 | pages= 334-40 | pmid=21375524 | doi=10.1111/j.1365-2141.2011.08596.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=21375524 }} &lt;/ref&gt;.<br /> * Patients may present with complaints of:<br /> ** Unexplained fever<br /> ** [[Weight loss]]<br /> ** Painless and progressive [[adenopathy]]<br /> ** Night sweats<br /> ** Gastric symptoms<br /> ** Urinary symptoms<br /> ** Nerve lesions<br /> ** Constant [[Fatigue (physical)|fatigue]]<br /> ** [[Pruritis|Itchy skin]]<br /> ** Reddened patches on the skin<br /> ** [[Cough]]<br /> ** [[Shortness of breath]]<br /> * Organ related symptoms develop depending on the metastatic spread of the lymphoma.<br /> * Patients may have a history of:<br /> ** Viral disease ([[Human Immunodeficiency Virus (HIV)|HIV]], [[Hepatitis B virus|HBV]], [[Hepatitis C|HCV]] or [[Epstein Barr virus|EBV]])<br /> ** [[Autoimmune diseases]]<br /> ** [[Immunodeficiency|Immunocompromised]] state<br /> <br /> == Complications ==<br /> * Skin reactions<br /> * [[Bone marrow]] suppresion<br /> * Second cancers<br /> * Gastric obstruction<br /> * Urethral obstruction<br /> * [[Renal insufficiency|Renal failure]]<br /> * [[Infertility]]<br /> * Heart problems (Heart failure, vavular defects, pericarditis)<br /> * Lung problems (Pleural effusion, lung mass)<br /> * Mediastinal mass<br /> * Immune system deficiency<br /> <br /> ==Prognosis==<br /> * Follicular Lymphoma International Prognostic Index (FLIPI) is used for the evaluation of prognosis&lt;ref name=&quot;pmid15126323&quot;&gt;{{cite journal| author=Solal-Céligny P, Roy P, Colombat P, White J, Armitage JO, Arranz-Saez R et al.| title=Follicular lymphoma international prognostic index. | journal=Blood | year= 2004 | volume= 104 | issue= 5 | pages= 1258-65 | pmid=15126323 | doi=10.1182/blood-2003-12-4434 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15126323 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7780151&quot;&gt;{{cite journal| author=Martin AR, Weisenburger DD, Chan WC, Ruby EI, Anderson JR, Vose JM et al.| title=Prognostic value of cellular proliferation and histologic grade in follicular lymphoma. | journal=Blood | year= 1995 | volume= 85 | issue= 12 | pages= 3671-8 | pmid=7780151 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7780151 }} &lt;/ref&gt;.<br /> <br /> * It includes the following:<br /> <br /> ** age &gt;60 years<br /> ** bone marrow involvement<br /> ** hemoglobin level &lt;12.0 g/dl<br /> ** greatest diameter of the largest involved node &gt;6 cm<br /> ** elevated serum β-2 microglobulin level<br /> * The FLIPI divides pateints into 3 groups:<br /> ** Low (0-1 risk factor)<br /> ** Intermediate (2 risk factors)<br /> ** High (≥ 3 risk factors)<br /> * The 10 year mortality of low group is 96%.<br /> * The 10 year mortality of intermediate group is 71%.<br /> * The 10 year mortality of high group is 37%.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_natural_history,_complications_and_prognosis&diff=1512497 2018-12-27T22:45:58Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> Follicular lymphoma presents in the age group of 60-65 with systemic symptoms of fever, weight loss, anorexia, night sweats and other organ dependent symptoms based on the metastatic spread of the lymphoma. Complications arise from the systemic effects of the lympoma and metastasis. The prognosis is evaluated from follicular lymphoma international prognostic index which divides patients into 3 groups.<br /> <br /> == Natural history ==<br /> * Follicular lymphoma presents in older age group people of age 60-65&lt;ref name=&quot;pmid23023713&quot;&gt;{{cite journal| author=Kridel R, Sehn LH, Gascoyne RD| title=Pathogenesis of follicular lymphoma. | journal=J Clin Invest | year= 2012 | volume= 122 | issue= 10 | pages= 3424-31 | pmid=23023713 | doi=10.1172/JCI63186 | pmc=3461914 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23023713 }} &lt;/ref&gt;&lt;ref name=&quot;pmid9166827&quot;&gt;{{cite journal| author=| title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project. | journal=Blood | year= 1997 | volume= 89 | issue= 11 | pages= 3909-18 | pmid=9166827 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=9166827 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7028244&quot;&gt;{{cite journal| author=Winberg CD, Nathwani BN, Bearman RM, Rappaport H| title=Follicular (nodular) lymphoma during the first two decades of life: a clinicopathologic study of 12 patients. | journal=Cancer | year= 1981 | volume= 48 | issue= 10 | pages= 2223-35 | pmid=7028244 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7028244 }} &lt;/ref&gt;&lt;ref name=&quot;pmid21375524&quot;&gt;{{cite journal| author=Fernández de Larrea C, Martínez-Pozo A, Mercadal S, García A, Gutierrez-García G, Valera A et al.| title=Initial features and outcome of cutaneous and non-cutaneous primary extranodal follicular lymphoma. | journal=Br J Haematol | year= 2011 | volume= 153 | issue= 3 | pages= 334-40 | pmid=21375524 | doi=10.1111/j.1365-2141.2011.08596.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=21375524 }} &lt;/ref&gt;.<br /> * Patients may present with complaints of:<br /> ** Unexplained fever<br /> ** Weight loss<br /> ** Painless and progressive adenopathy<br /> ** Night sweats<br /> ** Gastric symptoms<br /> ** Urinary symptoms<br /> ** Nerve lesions<br /> ** Constant [[Fatigue (physical)|fatigue]]<br /> ** [[Pruritis|Itchy skin]]<br /> ** Reddened patches on the skin<br /> ** [[Cough]]<br /> ** [[Shortness of breath]]<br /> * Organ related symptoms develop depending on the metastatic spread of the lymphoma.<br /> * Patients may have a history of:<br /> ** Viral disease (HIV, HBV, HCV or EBV)<br /> ** Autoimmune diseases<br /> ** Immunocompromised state<br /> <br /> == Complications ==<br /> * Skin reactions<br /> * Bone marrow suppresion<br /> * Second cancers<br /> * Gasrric obstruction<br /> * Urethral obstruction<br /> * Renal failure<br /> * Infertility<br /> * Heart problems (Heart failure, vavular defects, pericarditis)<br /> * Lung problems (Pleural effusion, lung mass)<br /> * Mediastinal mass<br /> * Immune system deficiency<br /> <br /> ==Prognosis==<br /> * Follicular Lymphoma International Prognostic Index (FLIPI) is used for the evaluation of prognosis&lt;ref name=&quot;pmid15126323&quot;&gt;{{cite journal| author=Solal-Céligny P, Roy P, Colombat P, White J, Armitage JO, Arranz-Saez R et al.| title=Follicular lymphoma international prognostic index. | journal=Blood | year= 2004 | volume= 104 | issue= 5 | pages= 1258-65 | pmid=15126323 | doi=10.1182/blood-2003-12-4434 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=15126323 }} &lt;/ref&gt;&lt;ref name=&quot;pmid7780151&quot;&gt;{{cite journal| author=Martin AR, Weisenburger DD, Chan WC, Ruby EI, Anderson JR, Vose JM et al.| title=Prognostic value of cellular proliferation and histologic grade in follicular lymphoma. | journal=Blood | year= 1995 | volume= 85 | issue= 12 | pages= 3671-8 | pmid=7780151 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=7780151 }} &lt;/ref&gt;.<br /> <br /> * It includes the following:<br /> <br /> ** age &gt;60 years<br /> ** bone marrow involvement<br /> ** hemoglobin level &lt;12.0 g/dl<br /> ** greatest diameter of the largest involved node &gt;6 cm<br /> ** elevated serum β-2 microglobulin level<br /> * The FLIPI divides pateints into 3 groups:<br /> ** Low (0-1 risk factor)<br /> ** Intermediate (2 risk factors)<br /> ** High (≥ 3 risk factors)<br /> * The 10 year mortality of low group is 96%.<br /> * The 10 year mortality of intermediate group is 71%.<br /> * The 10 year mortality of high group is 37%.<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_risk_factors&diff=1512488 2018-12-27T22:19:35Z

<p>Jogeet singh sekhon: /* Overview */</p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> The risk factors include [[Virus|viruses]], certain chemicals such as hair dyes and [[immunodeficiency]] states.<br /> ==Risk Factors==<br /> Risk factors for follicular lymphoma include&lt;ref name=&quot;pmid22754588&quot;&gt;{{cite journal| author=Ma S| title=Risk Factors of Follicular Lymphoma. | journal=Expert Opin Med Diagn | year= 2012 | volume= 6 | issue= 4 | pages= 323-333 | pmid=22754588 | doi=10.1517/17530059.2012.686996 | pmc=3384553 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22754588 }} &lt;/ref&gt;&lt;ref name=&quot;pmid23028387&quot;&gt;{{cite journal| author=Ambinder AJ, Shenoy PJ, Malik N, Maggioncalda A, Nastoupil LJ, Flowers CR| title=Exploring risk factors for follicular lymphoma. | journal=Adv Hematol | year= 2012 | volume= 2012 | issue= | pages= 626035 | pmid=23028387 | doi=10.1155/2012/626035 | pmc=3458409 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23028387 }} &lt;/ref&gt;:<br /> * Viruses:<br /> ** [[Epstein Barr virus|Epstein-Barr virus]] (EBV)<br /> ** [[Human T-cell lymphotropic virus]] (HTLV) type I,<br /> ** [[Herpes simplex virus|Herpesvirus]] associated with Kaposi sarcoma (ie, human herpesvirus [HHV]-8 )<br /> ** [[Hepatitis B]] and C viruses<br /> * Chemicals:<br /> ** Defoliants (eg, Agent Orange)<br /> ** Hair dyes<br /> <br /> * Immunodeficiency states:<br /> ** Congenital immunodeficiencies<br /> ** Infection with the human immunodeficiency virus ([[Human Immunodeficiency Virus (HIV)|HIV]]). Most lymphomas associated with HIV are intermediate-grade or high-grade lymphomas.<br /> ** Patients who have been on [[Immunosuppressive drug|immunosuppressant]] drugs after organ [[Organ transplant|transplantation]]. Most of these lymphomas are diffuse or high-grade lymphomas.<br /> ** [[Autoimmune diseases]]<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon https://www.wikidoc.org/index.php?title=Follicular_lymphoma_risk_factors&diff=1512485 2018-12-27T22:14:16Z

<p>Jogeet singh sekhon: </p> <hr /> <div>__NOTOC__<br /> {{Follicular lymphoma}}<br /> <br /> {{CMG}}; {{AE}} {{AS}}<br /> ==Overview==<br /> There are no established risk factors for follicular lymphoma.<br /> ==Risk Factors==<br /> Risk factors for follicular lymphoma include&lt;ref name=&quot;pmid22754588&quot;&gt;{{cite journal| author=Ma S| title=Risk Factors of Follicular Lymphoma. | journal=Expert Opin Med Diagn | year= 2012 | volume= 6 | issue= 4 | pages= 323-333 | pmid=22754588 | doi=10.1517/17530059.2012.686996 | pmc=3384553 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=22754588 }} &lt;/ref&gt;&lt;ref name=&quot;pmid23028387&quot;&gt;{{cite journal| author=Ambinder AJ, Shenoy PJ, Malik N, Maggioncalda A, Nastoupil LJ, Flowers CR| title=Exploring risk factors for follicular lymphoma. | journal=Adv Hematol | year= 2012 | volume= 2012 | issue= | pages= 626035 | pmid=23028387 | doi=10.1155/2012/626035 | pmc=3458409 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&amp;tool=sumsearch.org/cite&amp;retmode=ref&amp;cmd=prlinks&amp;id=23028387 }} &lt;/ref&gt;:<br /> * Viruses:<br /> ** Epstein-Barr virus (EBV)<br /> ** Human T-cell lymphotropic virus (HTLV) type I,<br /> ** Herpesvirus associated with Kaposi sarcoma (ie, human herpesvirus [HHV]-8 )<br /> ** Hepatitis B and C viruses<br /> * Chemicals:<br /> ** Defoliants (eg, Agent Orange)<br /> ** Hair dyes<br /> <br /> * Immunodeficiency states:<br /> ** Congenital immunodeficiencies<br /> ** Infection with the human immunodeficiency virus (HIV). Most lymphomas associated with HIV are intermediate-grade or high-grade lymphomas.<br /> ** Patients who have been on immunosuppressant drugs after organ transplantation. Most of these lymphomas are diffuse or high-grade lymphomas.<br /> ** Autoimmune diseases<br /> <br /> ==References==<br /> {{Reflist|2}}<br /> <br /> [[Category:Hematology]]<br /> [[Category:Types of cancer]]<br /> [[Category:Up-To-Date]]<br /> [[Category:Oncology]]<br /> [[Category:Medicine]]<br /> [[Category:Hematology]]<br /> [[Category:Immunology]]</div>

Jogeet singh sekhon