Villous adenoma: Difference between revisions
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* Dysplastic changes are present in the adenomas. | * Dysplastic changes are present in the adenomas. | ||
* Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma. | * Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma. | ||
* 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. | * 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.<ref name="pmid12725874">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12725874 }} </ref> | ||
* Pleomorphism and atypical mitoses are absent in low grade dysplasia. | * Pleomorphism and atypical mitoses are absent in low grade dysplasia. | ||
* The crypts maintain a resemblance to normal colon, without significant crowding, cribriform, or complex forms. | * 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. | ||
* As there are no lymphatic vessels in the lamina propria, lesions with high grade dysplasia are not associated with metastasis. | |||
* High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more "open" appearing nuclei with increasingly prominent nucleoli. | * High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more "open" appearing nuclei with increasingly prominent nucleoli. | ||
* Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. | * Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity. | ||
* 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 | * 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 <ref name="pmid30348703">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30348703 }} </ref>. | ||
* The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes. | * The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes<ref name="pmid15386327">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15386327 }} </ref>. | ||
* Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma. | * Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma. | ||
* The K-''ras'' oncogene, inactivation of tumor suppressor genes, the ''APC'' gene, on 5q, have important roles in adenoma formation. | * The K-''ras'' oncogene, inactivation of tumor suppressor genes, the ''APC'' gene, on 5q, have important roles in adenoma formation. | ||
| Line 40: | Line 41: | ||
**Polypoid or sessile mass | **Polypoid or sessile mass | ||
**Cauliflower-like in appearance\ | **Cauliflower-like in appearance\ | ||
* On microscopic histopathological analysis, characteristic findings of villous adenoma include: | * On microscopic histopathological analysis, characteristic findings of villous adenoma include<ref name="pmid30063919">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30063919 }} </ref>: | ||
**Nuclear changes at the surface of the [[mucosa]] | **Nuclear changes at the surface of the [[mucosa]] | ||
**Cigar-shaped (elongated) [[nucleus]] (length:width > 3:1) with nuclear [[hyperchromicity|hyperchromasia]] | **Cigar-shaped (elongated) [[nucleus]] (length:width > 3:1) with nuclear [[hyperchromicity|hyperchromasia]] | ||
| Line 46: | Line 47: | ||
**Nuclear crowding | **Nuclear crowding | ||
**Positive [[Ki-67]] | **Positive [[Ki-67]] | ||
* 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. | |||
==Causes== | ==Causes== | ||
| Line 66: | Line 68: | ||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of villous adenoma include: | Common risk factors in the development of villous adenoma include<ref name="pmid30370516">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30370516 }} </ref>: | ||
* [[Familial adenomatous polyposis]] | * [[Familial adenomatous polyposis]] | ||
* [[Peutz–Jeghers syndrome]] | * [[Peutz–Jeghers syndrome]] | ||
Revision as of 03:42, 6 February 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maria Fernanda Villarreal, M.D. [2]
Synonyms and keywords: Adenomatous polyps; VA; TVA
Overview
Villous adenoma (also known as adenomatous polyp) is a type of 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, 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, 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.
Historical Perspective
Villous adenoma was first discovered by Helwig in 1946.[1]
Classification
Villous adenoma may be classified into 3 subtypes according to histological appearance:[2]
- Tubular
- Tubulovillous
- Villous
Villous adenoma can be classified into 4 types according to the gross appearance.
- Flat
- Sessile
- Pedunculated
- Depressed
Pathophysiology
Pathogenesis
- The pathogenesis of villous adenoma is characterized by overgrowth of epithelial tissue with glandular characteristics.[2][3]
- Dysplastic changes are present in the adenomas.
- Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determines the progression of the adenoma.
- 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.[4]
- Pleomorphism and atypical mitoses are absent in low grade dysplasia.
- 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.
- As there are no lymphatic vessels in the lamina propria, lesions with high grade dysplasia are not associated with metastasis.
- High-grade dysplasia cytologically has increased nucleus to cytoplasm ratio, more significant loss of polarity, more "open" appearing nuclei with increasingly prominent nucleoli.
- Other features which distinguish a high grade from low-grade dysplasia include significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity.
- 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 [5].
- The progression of adenoma-to-carcinoma can also occur with activation of oncogenes and inactivation of tumor suppressor genes[6].
- Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.
- The K-ras oncogene, inactivation of tumor suppressor genes, the APC gene, on 5q, have important roles in adenoma formation.
- On gross pathology, characteristic findings of villous adenoma include:[2]
- Polypoid or sessile mass
- Cauliflower-like in appearance\
- On microscopic histopathological analysis, characteristic findings of villous adenoma include[7]:
- Nuclear changes at the surface of the mucosa
- Cigar-shaped (elongated) nucleus (length:width > 3:1) with nuclear hyperchromasia
- Large round nuclei
- Nuclear crowding
- Positive Ki-67
- 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.
Causes
Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is familial adenomatous polyposis.
Differentiating Villous Adenoma from Other Diseases
Villous adenoma must be differentiated from other diseases that cause abnormal growth of tissue projecting from a mucous membrane such as:
- Colorectal cancer
- Inflammatory fibroid polyp
Epidemiology and Demographics
Prevalence
The prevalence of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The prevalence of adenomas increases with age.
Age
Patients of all age groups may develop villous adenoma.
Gender
Males are more commonly affected with villous adenoma than females.
Race
Villous adenoma more commonly affects caucasians.
Risk Factors
Common risk factors in the development of villous adenoma include[8]:
- Familial adenomatous polyposis
- Peutz–Jeghers syndrome
- Turcot syndrome
- Juvenile polyposis syndrome
- Cowden disease
- Bannayan–Riley–Ruvalcaba syndrome (Bannayan-Zonana syndrome)
- Gardner's syndrome
Natural History, Complications and Prognosis
Natural History
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.[2]
Complications
Common complications of villous adenoma include:
- Bleeding
- Obstruction
- Bowel torsion
Prognosis
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%.
Diagnosis
Symptoms
Villous adenoma is commonly asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:
- Flatulence
- Abdominal pain
- Constipation
- Diarrhea
- Cramping
- Pencil-thin stools
Physical Examination
Patients with villous adenoma commonly appear well. Physical examination findings are often non-specific. Physical examination may demonstrate:
- Bright red blood on digital rectal examination
- Rectal mass
Laboratory Findings
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.[9]
Other diagnostic studies
Colonoscopy is the diagnostic modality of choice for villous adenoma. On colonoscopy, characteristic findings of villous adenoma include:[2]
- A sessile polyp
- Size can range from 0.5 cm to 5 cm
Alternative imaging studies include:
- CT colonography
- Video capsule endoscopy (less specific)
Treatment
Medical Therapy
There is no medical therapy for villous adenoma; the mainstay of therapy is surgical removal.
Surgery
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.[2]
Prevention
Primary Prevention
Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of familial adenomatous polyposis.
Secondary Prevention
Secondary prevention strategies include annual occult blood test and colonoscopy every ten years for patients above the age of 50.
References
- ↑ Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Osifo OD, Akhiwu W, Efobi CA (2009). "Small intestinal tubulovillous adenoma--case report and literature review". Niger J Clin Pract. 12 (2): 205–7. PMID 19764676.
- ↑ "StatPearls". 2018. PMID 29262150.
- ↑ Costantini M, Sciallero S, Giannini A, Gatteschi B, Rinaldi P, Lanzanova G; et al. (2003). "Interobserver agreement in the histologic diagnosis of colorectal polyps. the experience of the multicenter adenoma colorectal study (SMAC)". J Clin Epidemiol. 56 (3): 209–14. PMID 12725874.
- ↑ Rubio CA (2018). "Preliminary Report: Multiple Clusters of Proliferating Cells in Non-dysplastic Corrupted Colonic Crypts Underneath Conventional Adenomas". In Vivo. 32 (6): 1473–1475. doi:10.21873/invivo.11401. PMID 30348703.
- ↑ Komuta K, Batts K, Jessurun J, Snover D, Garcia-Aguilar J, Rothenberger D; et al. (2004). "Interobserver variability in the pathological assessment of malignant colorectal polyps". Br J Surg. 91 (11): 1479–84. doi:10.1002/bjs.4588. PMID 15386327.
- ↑ Goverde A, Wagner A, Bruno MJ, Hofstra RMW, Doukas M, van der Weiden MM; et al. (2018). "Routine Molecular Analysis for Lynch Syndrome Among Adenomas or Colorectal Cancer Within a National Screening Program". Gastroenterology. 155 (5): 1410–1415. doi:10.1053/j.gastro.2018.07.029. PMID 30063919.
- ↑ Jin Y, Yao L, Zhou P, Jin S, Wang X, Tang X; et al. (2018). "[Risk analysis of the canceration of colorectal large polyps]". Zhonghua Wei Chang Wai Ke Za Zhi. 21 (10): 1161–1166. PMID 30370516.
- ↑ Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016