Secondary amyloidosis epidemiology and demographics: Difference between revisions

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Latest revision as of 21:00, 30 October 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[2] Sahar Memar Montazerin, M.D.[3]

Overview

The incidence of AA amyloidosis is approximately 0.16 per 100,000 individuals in 2008 in the United kingdom. The mortality rate of systemic amyloidosis is approximately 100 per 100,000 deaths in developed countries. Secondary amyloidosis more commonly affects children. Men are more commonly affected by amyloidosis than women.

Epidemiology and Demographics

Incidence

The incidence of AA amyloidosis is approximately 0.16 per 100,000 individuals in 2008 in the United kingdom.^[1]

Prevalence

The prevalence of AA amyloidosis is 5,000 to 10,000 per 100,000 individuals with chronic inflammatory process per year worldwide.^[2]

Mortality rate

The mortality rate of systemic amyloidosis is approximately 100 per 100,000 deaths in developed countries.^[3]

Age

Secondary amyloidosis more commonly affects children.^[4]

Race

There is no racial predilection to secondary amyloidosis.

Gender

Men are more commonly affected by amyloidosis than women.^[5]

References

↑ Lane T, Pinney JH, Gilbertson JA, Hutt DF, Rowczenio DM, Mahmood S, Sachchithanantham S, Fontana M, Youngstein T, Quarta CC, Wechalekar AD, Gillmore JD, Hawkins PN, Lachmann HJ (September 2017). "Changing epidemiology of AA amyloidosis: clinical observations over 25 years at a single national referral centre". Amyloid. 24 (3): 162–166. doi:10.1080/13506129.2017.1342235. PMID 28686088.
↑ Koivuniemi, Riitta; Paimela, Leena; Suomalainen, Risto; Törnroth, Tom; Leirisalo-Repo, Marjatta (2009). "Amyloidosis is frequently undetected in patients with rheumatoid arthritis". Amyloid. 15 (4): 262–268. doi:10.1080/13506120802524676. ISSN 1350-6129.
↑ Pepys MB (2006). "Amyloidosis". Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
↑ Bilginer, Yelda; Akpolat, Tekin; Ozen, Seza (2011). "Renal amyloidosis in children". Pediatric Nephrology. 26 (8): 1215–1227. doi:10.1007/s00467-011-1797-x. ISSN 0931-041X.
↑ Shin YM (March 2011). "Hepatic amyloidosis". Korean J Hepatol. 17 (1): 80–3. doi:10.3350/kjhep.2011.17.1.80. PMC 3304630. PMID 21494083.

Template:WH Template:WS

[pmid28686088-1] Lane T, Pinney JH, Gilbertson JA, Hutt DF, Rowczenio DM, Mahmood S, Sachchithanantham S, Fontana M, Youngstein T, Quarta CC, Wechalekar AD, Gillmore JD, Hawkins PN, Lachmann HJ (September 2017). "Changing epidemiology of AA amyloidosis: clinical observations over 25 years at a single national referral centre". Amyloid. 24 (3): 162–166. doi:10.1080/13506129.2017.1342235. PMID 28686088.

[KoivuniemiPaimela2009-2] Koivuniemi, Riitta; Paimela, Leena; Suomalainen, Risto; Törnroth, Tom; Leirisalo-Repo, Marjatta (2009). "Amyloidosis is frequently undetected in patients with rheumatoid arthritis". Amyloid. 15 (4): 262–268. doi:10.1080/13506120802524676. ISSN 1350-6129.

[pmid16409147-3] Pepys MB (2006). "Amyloidosis". Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.

[BilginerAkpolat2011-4] Bilginer, Yelda; Akpolat, Tekin; Ozen, Seza (2011). "Renal amyloidosis in children". Pediatric Nephrology. 26 (8): 1215–1227. doi:10.1007/s00467-011-1797-x. ISSN 0931-041X.

[pmid21494083-5] Shin YM (March 2011). "Hepatic amyloidosis". Korean J Hepatol. 17 (1): 80–3. doi:10.3350/kjhep.2011.17.1.80. PMC 3304630. PMID 21494083.

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@@ Line 1: / Line 1: @@
 __NOTOC__
-{{Amyloidosis}}
+{{Secondary amyloidosis}}
-{{CMG}}; {{AE}}{{SHH}}{{Sab}}
+{{CMG}}; {{AE}} {{SHH}} {{Sahar}}
 == Overview ==
-[[Amyloid]] is an abnormal insoluble [[extracellular]] [[protein]] that deposits in the different tissues and causes organic dysfunction and a wide variety of clinical syndromes. In systemic amyloidosis, [[amyloid]] gradually accumulate and [[amyloid]] deposition is widespread in the viscera, [[blood vessel]] walls, and in the different [[Connective tissue|connective tissues]]. [[AL amyloidosis|Primary (AL) amyloidosis)]] is the most common type of amyloidosis. It results from aggregation and deposition of monoclonal [[Immunoglobulin|immunoglobulin (Ig)]] [[Light chain|light chains]] that usually produced by [[plasma cell]] clones. [[AA amyloidosis|Secondary amyloidosis]] is associated with chronic [[inflammation]] (such as [[tuberculosis]] or [[rheumatoid arthritis]]). Hereditary (or familial) amyloidosis are [[Autosome|autosomal]] [[Dominance relationship|dominant]] diseases that [[inherited]] variant [[Protein|proteins]] cause the production and deposition of [[amyloid]] fibrils. Some [[Neurodegenerative disease|neurodegenerative disorders]] such as [[Parkinson's disease]], [[Alzheimer's disease|Alzheimer]], and [[Huntington's disease]] may occur in localised amyloidosis. On microscopic pathology, typical green [[birefringence]] under [[Polarization|polarized]] light after [[Congo red]] staining (appears in red under normal light).
+The [[incidence]] of AA amyloidosis is approximately 0.16 per 100,000 individuals in 2008 in the United kingdom. The [[mortality rate]] of systemic amyloidosis is approximately 100 per 100,000 deaths in developed countries. Secondary amyloidosis more commonly affects children. Men are more commonly affected by amyloidosis than women.
+==Epidemiology and Demographics==
+===Incidence===
+* The [[incidence]] of AA amyloidosis is approximately 0.16 per 100,000 individuals in 2008 in the United kingdom.<ref name="pmid28686088">{{cite journal |vauthors=Lane T, Pinney JH, Gilbertson JA, Hutt DF, Rowczenio DM, Mahmood S, Sachchithanantham S, Fontana M, Youngstein T, Quarta CC, Wechalekar AD, Gillmore JD, Hawkins PN, Lachmann HJ |title=Changing epidemiology of AA amyloidosis: clinical observations over 25 years at a single national referral centre |journal=Amyloid |volume=24 |issue=3 |pages=162–166 |date=September 2017 |pmid=28686088 |doi=10.1080/13506129.2017.1342235 |url=}}</ref>
+===Prevalence===
+* The [[prevalence]] of AA amyloidosis is 5,000 to 10,000 per 100,000 individuals with chronic [[inflammatory]] process per year worldwide.<ref name="KoivuniemiPaimela2009">{{cite journal|last1=Koivuniemi|first1=Riitta|last2=Paimela|first2=Leena|last3=Suomalainen|first3=Risto|last4=Törnroth|first4=Tom|last5=Leirisalo-Repo|first5=Marjatta|title=Amyloidosis is frequently undetected in patients with rheumatoid arthritis|journal=Amyloid|volume=15|issue=4|year=2009|pages=262–268|issn=1350-6129|doi=10.1080/13506120802524676}}</ref>
+===Mortality rate===
+* The [[mortality rate]] of systemic amyloidosis is approximately 100 per 100,000 deaths in developed countries.<ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
+===Age===
+* Secondary amyloidosis more commonly affects children.<ref name="BilginerAkpolat2011">{{cite journal|last1=Bilginer|first1=Yelda|last2=Akpolat|first2=Tekin|last3=Ozen|first3=Seza|title=Renal amyloidosis in children|journal=Pediatric Nephrology|volume=26|issue=8|year=2011|pages=1215–1227|issn=0931-041X|doi=10.1007/s00467-011-1797-x}}</ref>
+===Race===
+* There is no racial predilection to secondary amyloidosis.
+===Gender===
+* Men are more commonly affected by amyloidosis than women.<ref name="pmid21494083">{{cite journal |vauthors=Shin YM |title=Hepatic amyloidosis |journal=Korean J Hepatol |volume=17 |issue=1 |pages=80–3 |date=March 2011 |pmid=21494083 |pmc=3304630 |doi=10.3350/kjhep.2011.17.1.80 |url=}}</ref>
-== Pathophysiology ==
+==References==
+{{Reflist|2}}
-*[[Amyloid]] is an abnormal insoluble [[extracellular]] [[protein]] that deposits in the different tissues and causes organic dysfunction and a wide variety of clinical syndromes.<ref name="pmid26719234">{{cite journal |vauthors=Wechalekar AD, Gillmore JD, Hawkins PN |title=Systemic amyloidosis |journal=Lancet |volume=387 |issue=10038 |pages=2641–2654 |date=June 2016 |pmid=26719234 |doi=10.1016/S0140-6736(15)01274-X |url=}}</ref>
+[[Category:Needs content]]
-*These abnormal [[Amyloid|amyloids]] are derived from misfolding and aggregation of normally soluble [[Protein|proteins]].
+[[Category:Disease]]
-*[[Amyloid]] deposition can disrupt tissue structure of involved organ and consequently leads to organ failure.<ref name="pmid267192342">{{cite journal |vauthors=Wechalekar AD, Gillmore JD, Hawkins PN |title=Systemic amyloidosis |journal=Lancet |volume=387 |issue=10038 |pages=2641–2654 |date=June 2016 |pmid=26719234 |doi=10.1016/S0140-6736(15)01274-X |url=}}</ref>
+[[Category:Rheumatology]]
+[[Category:Cardiology]]
+[[Category:Endocrinology]]
-===Systemic Amyloidosis===
-*In systemic amyloidosis, [[amyloid]] gradually accumulates and [[amyloid]] deposition is widespread in the viscera, [[blood vessel]] walls, and different [[Connective tissue|connective tissues]].<ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
-====Secondary Amyloidosis (AA)====
-*[[AA amyloidosis|Secondary amyloidosis]] occurs as a reaction to an existing illness.
-*[[AA amyloidosis|Secondary amyloidosis]] is associated with chronic [[inflammation]] (such as [[tuberculosis]] or [[rheumatoid arthritis]]).<ref name="pmid116772762">{{cite journal |vauthors=Khan MF, Falk RH |title=Amyloidosis |journal=Postgrad Med J |volume=77 |issue=913 |pages=686–93 |date=November 2001 |pmid=11677276 |pmc=1742163 |doi= |url=}}</ref>
-*[[AA amyloidosis|Secondary or reactive amyloidosis (AA)]] comprises approximately 45% of the systemic amyloidoses.
-*[[Pathogenesis]] of [[AA amyloidosis|secondary amyloidosis]] is multifactorial, including:
-**[[Primary structure]] of the [[precursor]] protein
-**Acute phase response
-**Nonfibril [[Protein|proteins]] ([[amyloid]] P component, [[Apolipoprotein E|apo E]], [[Glycosaminoglycan|GAGs]], [[Proteoglycan|proteoglycans]] and [[basement membrane]] [[Protein|proteins]])
-**[[Receptor (biochemistry)|Receptors]]
-**[[Lipid metabolism]]
-**[[Protease|Proteases]]
-== Associated Conditions ==
-Conditions associated with amyloidosis include:<ref name="pmid8757765">{{cite journal |vauthors=Hofstra RM, Sijmons RH, Stelwagen T, Stulp RP, Kousseff BG, Lips CJ, Steijlen PM, Van Voorst Vader PC, Buys CH |title=RET mutation screening in familial cutaneous lichen amyloidosis and in skin amyloidosis associated with multiple endocrine neoplasia |journal=J. Invest. Dermatol. |volume=107 |issue=2 |pages=215–8 |date=August 1996 |pmid=8757765 |doi=10.1111/1523-1747.ep12329651 |url=}}</ref>
-* MEN2A
-== Gross Pathology ==
-On gross pathology, the organs affected by amyloidosis can be characterized by the following features:
-*Porcelain like or waxy appearance
-*Enlargement
-===Images===
-[[File:Amyloidosis (4867136708).jpg|300px|left|thumb|Nodular deposits of amyloid on the pleural surfaces.<ref>By Yale Rosen from USA - Amyloidosis, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31127928</ref>]]
-[[File:Amyloidosis, Node, Gross.jpg|400px|center|thumb|Cut section of an inguinal lymph node showing firm and waxy consistency.<ref>By Ed Uthman, MD - https://www.flickr.com/photos/euthman/377537238/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=1629764</ref>]]
-[[File:Amyloidosis, Node, Lugol's Reaction.jpg|300px|left|thumb|A slice of the affected node (left) has turned black after treatment with Lugol's solution. A piece of normal myometrium (right) treated similarly with no reaction is also shown.<ref>By Ed Uthman, MD - https://www.flickr.com/photos/euthman/377538012/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=1629740</ref>]]
-<br style="clear:left">
-==Microscopic Pathology==
-On microscopic histopathological analysis, amyloidosis is characterized by:<ref name="pmid116772762" /><ref name="pmid119640392">{{cite journal |vauthors=Röcken C, Shakespeare A |title=Pathology, diagnosis and pathogenesis of AA amyloidosis |journal=Virchows Arch. |volume=440 |issue=2 |pages=111–122 |date=February 2002 |pmid=11964039 |doi=10.1007/s00428-001-0582-9 |url=}}</ref>
-*Green [[birefringence]] under [[Polarization|polarized]] light after [[Congo red]] staining (appears red under normal light)
-*Linear non-branching [[Fibril|fibrils]] (indefinite length with an approximately same diameter)
-*Distinct [[X-rays|X-ray]] diffraction pattern consistent with Pauling's model of a cross-beta fibril
-===Images===
-[[File:Small bowel duodenum with amyloid deposition congo red 10X.jpg|300px|left|thumb|Small bowel duodenum with amyloid deposition Congo red.<ref>By Michael Feldman, MD, PhDUniversity of Pennsylvania School of Medicine - http://www.healcentral.org/healapp/showMetadata?metadataId=38717, CC BY 2.0, https://commons.wikimedia.org/w/index.php?curid=870218</ref>]]
-[[File:Amyloidosis, Node, Congo Red.jpg|300px|center|thumb|Amyloidosis (black arrows) in a lymph node after staining with Congo Red.<ref>By Ed Uthman, MD - https://www.flickr.com/photos/euthman/377559787/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=1629716</ref>]]
-[[File:Amyloidosis, lymph node, polarizer.jpg|300px|left|thumb|Green [[birefringence]] under [[Polarization|polarized]] light.<ref>By Ed Uthman, MD - https://www.flickr.com/photos/euthman/377559955/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=1629705</ref>]]
-<br style="clear:left">
-== References ==
-{{reflist|2}}
 {{WH}}
 {{WS}}