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__NOTOC__
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{{SI}}                                                                 
{{Villous adenoma}}                                                                 
{{CMG}}; {{AE}} {{MV}}; {{TarekNafee}}
{{CMG}}; {{AE}} {{JSS}} {{MV}}


{{SK}} Adenomatous polyps; VA; TVA
{{SK}} Adenomatous polyps; VA; TVA
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==Overview==
==Overview==


'''Villous adenoma''' (also known as adenomatous polyp) is a type of [[polyp (medicine)|polyp]] that grows in the [[colon]] and other places in the [[gastrointestinal tract]] and may have a [[malignant]] ([[cancerous]]) transformation.<ref>[http://www.cancer.gov/Templates/db_alpha.aspx?CdrID=44809 Villous adenoma]</ref> Villous adenoma was first discovered by Helwig in 1946.<ref name=":0">Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95</ref>  According to the World Health Organization, villous adenoma can be classified into 3 groups: tubular, tubulovillous, and villous (most common). Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. The estimated risk of malignancy among villous adenomas is between 15 and 25%. Genes associated in the development of villous adenoma, include: APC gene, TP53 gene, K-ras gene, and BAT-26 gene. The prevalence of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most important risk factor in the development of villous adenoma is familiar syndromes (e.g. [[Turcot syndrome|Turcot syndrome,]] [[Juvenile polyposis syndrome|juvenile polyposis syndrome, and]] [[Cowden disease]]). Surgical removal is the mainstay of therapy for villous adenoma. Cautery snare in conjunction with exploratory colonoscopy is the most common approach to the treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodical screening for patients with family history of familial adenomatous polyposis. According to the guidelines established by the American Cancer Society, individuals who reach the age of 50 should perform an occult blood test yearly.
'''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]]<nowiki/>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.


==Historical Perspective==
==Historical Perspective==
Villous adenoma was first discovered by Helwig in 1946.<ref name=":0">Helwig E.B. Adenoma of the large bowel in children. American Journal of Diseases in Children. 1946;72:289–95</ref>
Villous adenoma was first discovered by Helwig in 1946.<ref name=":0">Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95</ref>


==Classification==
==Classification==
Villous adenoma may be classified according to the World Health Organization into 3 groups:<ref name="pmid19764676">{{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=}}</ref>
[[Colon polyps|Colon polyp]]<nowiki/>s are classified into 3 subtypes according to their histological appearance:<ref name="pmid19764676">{{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=}}</ref>
*Tubular
*[[Tubular]]
*Tubulovillous
*Tubulovillous
*Villous (most common)
*[[Villous carcinoma|Villous]]
Villous adenoma is classified into 4 types according to the gross appearance:<ref name="ShussmanWexner2014">{{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}}</ref>
* Flat
* Sessile
* Pedunculated
* Depressed
Villous adenoma is classified into 2 types according to [[dysplasia]]:
* Low grade dysplasia
* High grade dysplasia


==Pathophysiology==
==Pathophysiology==
===Pathogenesis===
===Pathogenesis===
The pathogenesis of villous adenoma is characterized by:<ref name="pmid19764676">{{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=}}</ref> Villous adenoma arises from overgrowth of epithelial tissue with glandular characteristics.
* Villous adenoma is a type of colon polyp.<ref name="pmid18314605">{{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=}}</ref><ref name="ShussmanWexner2014">{{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}}</ref><ref name="SinghZorrón Cheng Tao Pu2016">{{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}}</ref><ref name="KahiVemulapalli2015">{{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}}</ref>
===Genetics===
* The pathogenesis of villous adenoma is characterized by overgrowth of [[epithelial]] tissue with [[glandular]] characteristics.<ref name="pmid19764676">{{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=}}</ref><ref name="pmid29262150">{{cite journal| author=| title=StatPearls | journal= | year= 2018 | volume=  | issue=  | pages=  | pmid=29262150 | doi= | pmc= | url= }} </ref>
Genes associated with the development of villous adenoma include:<ref name="pmid19764676">{{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=}}</ref>
* [[Dysplasia|Dysplastic]] changes are present in the adenomas.
*[[APC gene]]
* Multiple genetic [[Mutation|mutations]] result in the transition from normal [[Mucous membrane|mucosa]] to adenoma to severe [[dysplasia]] and finally to [[carcinoma]].
*[[TP53|TP53 gene]]
* Low grade or high-grade [[dysplasia]], which indicates the level of maturation of the epithelium determine the progression of the adenoma.
*[[KRAS]] gene
* Features of low grade dysplasia are:
*BAT-26 gene
** 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]].<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 [[Mitosis|mitoses]] are absent.
===Gross Pathology===
** 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]].
On gross pathology, characteristic findings of villous adenoma include:<ref name="pmid19764676">{{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=}}</ref>
** As there are no [[Lymphatic system|lymphatic]] vessels in the lamina propria, lesions with low grade dysplasia are not associated with metastasis.
*Polypoid or sessile mass
* Features of high grade dysplasia are:
*Cauliflower-like in appearance
** The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent [[nucleoli]].
===Microscopic Pathology===
** Significant [[pleomorphism]], rounded nuclei, atypical mitoses, and significant loss of polarity.
On microscopic histopathological analysis, characteristic findings of villous adenoma include:
** The crypts are cribriform and crowded with back-to-back [[glandular]] tissue <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>.
*Nuclear changes at the surface of the [[mucosa]]
** These adenomas have a significant risk of metastasis as the lesions can invade into the lamina propria through basement membrane destruction.
*Cigar-shaped (elongated) [[nucleus]] (length:width > 3:1) with nuclear [[hyperchromasia]]
* Villous adenoma can lead to [[adenocarcinoma]] of the colon.
*Large round [[nuclei]]
* The progression of adenoma-to-carcinoma is dependent on the activation of [[Oncogene|oncogenes]] and inactivation of [[Tumor suppressor gene|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>
*Nuclear crowding
* Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.
*Positive [[Ki-67]]
* The genes involved in adenoma formation are:
** [[Oncogene|K-ras oncogene]]
** Tumor suppressor [[p53]] gene
** [[APC]] gene on [[chromosome 5]] associated with [[FAP|familial automatosis polyposis]] syndrome and [[Gardner's syndrome]]
** [[STK11]] (LBK1) gene, located on [[chromosome 19]] associated with [[Peutz-Jeghers syndrome]]
** [[Mothers against decapentaplegic homolog 4|SMAD4]] on [[chromosome 8]] associated with [[juvenile polyposis syndrome]]
* 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]].
[[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 style="clear:left" />


==Causes==
==Causes==
Villous adenomas are commonly idiopathic. The most common known cause of villous adenoma is [[familial adenomatous polyposis]].
The cause of villous adenoma is not yet identified.


==Differentiating Villous Adenoma from Other Diseases==
==Differentiating Villous Adenoma from Other Diseases==
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* [[Colorectal cancer]]
* [[Colorectal cancer]]
* Inflammatory fibroid polyp
* Inflammatory fibroid polyp
* Tubular adenoma
* Tubulovillous adenoma
* Hyperplastic polyp


==Epidemiology and Demographics==
==Epidemiology and Demographics==
===Prevalence===
===Prevalence===
The prevalence of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The prevalence of adenomas increases with age.  
* The [[prevalence]] of villous adenoma is approximately 3.5 per 100,000 individuals worldwide.<ref name="pmid15666099">{{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=}}</ref> 
 
===Age===
===Age===
Patients of all age groups may develop villous adenoma.
* Patients of all age groups may develop villous adenoma but the risk increases with age.
 
===Gender===
===Gender===
Males are more commonly affected with villous adenoma than females.  
* Males are more commonly affected with villous adenoma than females.  
 
===Race===
===Race===
Villous adenoma more commonly affects individuals of the Caucasian race.
* African Americans are more prone to develop villous adenoma.
 
=== Region ===
* Villous adenomas is common worldwide and has no regional predilection.


==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><ref name="pmid12376501">{{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=}}</ref>:
* Age more than 50 years
* African American race
* Male sex
* [[Inflammatory bowel disease]]
* [[Alcoholism|Alcohol abuse]]
* [[Obesity]]
* Lack of [[Physical exercise|exercise]]
* [[Diet (nutrition)|Diet]] high in red meats and processed meats
* Low [[Fiber (food)|fiber]] intake
* Low [[calcium]] intake
* Low [[Folic Acid|folate]] intake
* [[Diabetes mellitus type 2|Type 2 diabetes mellitus]]
* [[Familial adenomatous polyposis]]
* [[Familial adenomatous polyposis]]
* [[Peutz–Jeghers syndrome]]
* [[Peutz–Jeghers syndrome]]
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* [[Gardner's syndrome]]
* [[Gardner's syndrome]]


== Natural History, Complications and Prognosis==
== Natural History, Complications, and Prognosis==
===Natural History===
===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]].<ref name="pmid19764676">{{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=}}</ref>
* The majority of patients with villous adenoma remain asymptomatic for years.<ref name="Bonnington2016">{{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}}</ref>
* They are usually found accidentally on routine [[Colonoscopy|colonoscopic]] surveillance.
* Early clinical features may include [[flatulence]], [[bloating]], and [[abdominal pain]].
* If left untreated, patients with villous adenoma may progress to develop [[colorectal cancer]].<ref name="pmid19764676">{{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=}}</ref>
* The patients may have a previous history of [[colon polyps]].
* Family history of [[Colorectal cancer|colon cancer]] or [[colon polyps]].
 
===Complications===
===Complications===
Common complications of villous adenoma include:
Common complications of villous adenoma include:
*Bleeding
*[[Gastrointestinal bleeding]]
*Obstruction
*[[Bowel obstruction|Intestinal obstruction]]
*Bowel torsion
*Progression to [[colorectal cancer]]
 
===Prognosis===
===Prognosis===
Prognosis is generally good and the 5-year mortality of patients with villous adenoma 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%.
* The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%.<ref name="BettingtonWalker2013">{{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}}</ref>
* Prognosis becomes poor with [[malignant]] transformation of the lesion.  
* Multiple villous adenomas may suggest [[Genetic disorder|genetic disorders]] and prognosis is poor in these cases.


== Diagnosis ==
== Diagnosis ==


=== Symptoms ===
=== Diagnostic study of choice ===
Villous adenoma is usually asymptomatic. Villous adenoma symptoms are often non-specific. Symptoms of villous adenoma may include:
* [[Biopsy]] of the lesion is the diagnostic study of choice<ref name="ShussmanWexner2014">{{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}}</ref>.
*Flatulence
* Villous adenoma is detected on [[colonoscopy]] or [[sigmoidoscopy]].
*Abdominal pain  
 
*Constipation
=== History and Symptoms ===
*Diarrhea
Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms:<ref name="JohnsonKisiel2017">{{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}}</ref><ref name="ShussmanWexner2014">{{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}}</ref>
*Cramping
*[[Flatulence]]
*[[Abdominal pain]]
*[[Constipation]]
*[[Diarrhea]]
*[[Cramping]]
*[[Gastrointestinal bleeding|Blood in stools]]
*[[Weight loss]]
*Change in bowel habits
*[[Fatigue]]


=== Physical Examination ===
=== Physical Examination ===
Patients with villous adenoma usually are well-appearing. Physical examination findings are often non-specific. Physical examination may demonstrate:
Patients with villous adenoma usually appear well but may have the following signs on examination.
*Rectal bleeding
*[[Pallor]] due to [[Occult blood|occult]] bleeding
*Rectal mass
*[[Tenderness (medicine)|Abdominal tenderness]]
*Pencil-thin stools
*Bright red blood on [[Rectal examination|digital rectal examination]]
*[[Rectal masses|Rectal mass]] on [[Rectal examination|digital rectal examination]]


=== Laboratory Findings ===
=== Laboratory Findings ===
There are no specific laboratory findings associated with villous adenoma. In some cases, patients with villous adenoma may demonstrate hypokalemia.<ref name="wiki"> Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 </ref>
Laboratory findings associated with villous adenoma are:
* Positive [[fecal occult blood test]]
* [[Hypokalemia]]<ref name="wiki">Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016 </ref>
* [[Anemia]]
 
===Electrocardiogram===
 
=== X-ray ===
 
=== Echocardiography or Ultrasound ===
 
=== CT scan ===
 
=== MRI ===
 
=== Other Imaging Findings ===
 
=== Other Diagnostic Studies ===
On [[colonoscopy]] and [[sigmoidoscopy]], villous adenoma is visualised as a [[polyp]].


===Imaging and Diagnostic Findings===
Alternative imaging studies include:  
Colonoscopy is the diagnostic modality of choice for villous adenoma. On colonoscopy, characteristic findings of villous adenoma include:<ref name="pmid19764676">{{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=}}</ref>
*CT colonography
*A sessile polyp
*Video [[capsule endoscopy]]
*Size can range from 0.5 cm to 5 cm
Other imaging studies include:  
*Computed tomographic colonography
*Video capsule endoscopy (less specific)


== Treatment ==
== Treatment ==
=== Medical Therapy ===
=== Medical Therapy ===
There is no treatment for villous adenoma; the mainstay of therapy is surgical removal.  
* There is no medical therapy for villous adenoma.
* Surgical removal of the adenoma is the mainstay of treatment.
* However, [[aspirin]] 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer.<ref name="pmid27064573">{{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=}}</ref>


=== Surgery ===
=== 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.<ref name="pmid19764676">{{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=}}</ref>
* Surgical removal is the mainstay of therapy for villous adenoma.<ref name="Winawer2015">{{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}}</ref><ref name="RameshshankerWilson2016">{{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}}</ref>
* The removal of adenoma is known as [[polypectomy]] and is done through [[colonoscopy]] by [[Endoscopy|endoscopic]] forceps snare.
* The removed adenoma must be sent for [[biopsy]].
*
{{#ev:youtube|ClgRkyhaJZw}}
 
=== Primary Prevention ===
Effective measures for the primary prevention of villous adenoma include:
* Periodic screening for polyps in patients with family history of :
** [[Familial adenomatous polyposis]]
** [[Peutz–Jeghers syndrome]]
** [[Turcot syndrome]]
** [[Juvenile polyposis syndrome]]
** [[Cowden disease]]
** [[Bannayan–Riley–Ruvalcaba syndrome]] ([[Bannayan-Riley-Ruvalcaba syndrome|Bannayan-Zonana syndrome]])
** [[Gardner's syndrome]]
* Exercise
* [[Smoking cessation]]
* Avoid alcohol
* High fiber diet


=== Prevention ===
===Secondary Prevention===
Effective measures for the primary prevention of villous adenoma include periodic screening for patients with family history of familial adenomatous polyposis. According to the guidelines established by the American Cancer Society, individuals who reach the age of 50 should perform an occult blood test yearly, a colonoscopy every 10 years, or a flexible sigmoidoscopy every 3 to 5 years. Once diagnosed and successfully treated, patients with villous adenoma are followed-up every 12 to 24 months.
[[Aspirin]] 75mg PO daily.
* Annual [[Fecal occult blood|fecal occult blood test]]<ref name="pmid22763141">{{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&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22763141  }} </ref>
* [[Colonoscopy]] every ten years for patients above the age of 50 with no family history of [[Colorectal cancer|colon cancer]] or no history of [[colon polyps]]
* [[Colonoscopy]] at the age of 40 or 10 years before the age of [[cancer]] diagnosis in a relative with [[Colorectal cancer|colon cancer]] and repeat every 3-5 years
* [[Colonoscopy]] after [[polypectomy]]:
** Every 5 years if 1-2 adenomas present or size <1 cm
** Every 3 years if 3-10 adenomas present or when size of adenoma is 1-2 cm
** Every 1-2 years if >10 adenomas present or if size is >2cm
** Every 2-6 months if signs of [[adenocarcinoma]] present


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Up-To-Date]]
[[Category:Oncology]]
[[Category:Medicine]]
[[Category:Gastroenterology]]
[[Category:Surgery]]

Latest revision as of 18:22, 22 May 2019


Villous adenoma Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2] Maria Fernanda Villarreal, M.D. [3]

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 malignanttransformation. 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 epithelial tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include APC, TP53, 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, 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.

Historical Perspective

Villous adenoma was first discovered by Helwig in 1946.[1]

Classification

Colon polyps are classified into 3 subtypes according to their histological appearance:[2]

Villous adenoma is classified into 4 types according to the gross appearance:[3]

  • Flat
  • Sessile
  • Pedunculated
  • Depressed

Villous adenoma is classified into 2 types according to dysplasia:

  • Low grade dysplasia
  • High grade dysplasia

Pathophysiology

Pathogenesis

  • Villous adenoma is a type of colon polyp.[4][3][5][6]
  • The pathogenesis of villous adenoma is characterized by overgrowth of epithelial tissue with glandular characteristics.[2][7]
  • Dysplastic changes are present in the adenomas.
  • Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.
  • Low grade or high-grade dysplasia, which indicates the level of maturation of the epithelium determine the progression of the adenoma.
  • Features of low grade dysplasia are:
    • The cytological features include crowded, pseudo-stratification to early stratification of spindled or elongated nuclei which occupy the basal half of the cytoplasm.[8]
    • Pleomorphism and atypical mitoses are absent.
    • 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 low grade dysplasia are not associated with metastasis.
  • Features of high grade dysplasia are:
    • The cytological features include increased nucleus to cytoplasm ratio, more significant loss of polarity and nuclei with increasingly prominent nucleoli.
    • Significant pleomorphism, rounded nuclei, atypical mitoses, and significant loss of polarity.
    • The crypts are cribriform and crowded with back-to-back glandular tissue [9].
    • These adenomas have a significant risk of metastasis as the lesions can invade into the lamina propria through basement membrane destruction.
  • Villous adenoma can lead to adenocarcinoma of the colon.
  • The progression of adenoma-to-carcinoma is dependent on the activation of oncogenes and inactivation of tumor suppressor genes.[10]
  • Multiple genetic mutations result in the transition from normal mucosa to adenoma to severe dysplasia and finally to carcinoma.
  • The genes involved in adenoma formation are:
  • 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.
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


Causes

The cause of villous adenoma is not yet identified.

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
  • Tubular adenoma
  • Tubulovillous adenoma
  • Hyperplastic polyp

Epidemiology and Demographics

Prevalence

  • The prevalence of villous adenoma is approximately 3.5 per 100,000 individuals worldwide.[11]

Age

  • Patients of all age groups may develop villous adenoma but the risk increases with age.

Gender

  • Males are more commonly affected with villous adenoma than females.

Race

  • African Americans are more prone to develop villous adenoma.

Region

  • Villous adenomas is common worldwide and has no regional predilection.

Risk Factors

Common risk factors in the development of villous adenoma include[12][13]:

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of villous adenoma include:

Prognosis

  • The prognosis of villous adenoma is generally good and the 5-year mortality is approximately 89%.[15]
  • Prognosis becomes poor with malignant transformation of the lesion.
  • Multiple villous adenomas may suggest genetic disorders and prognosis is poor in these cases.

Diagnosis

Diagnostic study of choice

History and Symptoms

Villous adenoma is commonly asymptomatic but sometimes patients may present with the following symptoms:[16][3]

Physical Examination

Patients with villous adenoma usually appear well but may have the following signs on examination.

Laboratory Findings

Laboratory findings associated with villous adenoma are:

Electrocardiogram

X-ray

Echocardiography or Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

On colonoscopy and sigmoidoscopy, villous adenoma is visualised as a polyp.

Alternative imaging studies include:

Treatment

Medical Therapy

  • There is no medical therapy for villous adenoma.
  • Surgical removal of the adenoma is the mainstay of treatment.
  • However, aspirin 75mg PO per day is recommended to prevent recurrence of the adenoma and progression to colorectal cancer.[18]

Surgery

{{#ev:youtube|ClgRkyhaJZw}}

Primary Prevention

Effective measures for the primary prevention of villous adenoma include:

Secondary Prevention

Aspirin 75mg PO daily.

References

  1. ↑ Helwig E.B. Adenoma of the large bowel in children. . American Journal of Diseases in Children. 1946;72:289–95
  2. ↑ 2.0 2.1 2.2 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.
  3. ↑ 3.0 3.1 3.2 3.3 Shussman, N.; Wexner, S. D. (2014). "Colorectal polyps and polyposis syndromes". Gastroenterology Report. 2 (1): 1–15. doi:10.1093/gastro/got041. ISSN 2052-0034.
  4. ↑ Rüschoff J, Aust D, Hartmann A (2007). "[Colorectal serrated adenoma: diagnostic criteria and clinical implications]". Verh Dtsch Ges Pathol (in German). 91: 119–25. PMID 18314605.
  5. ↑ Singh, Rajvinder; Zorrón Cheng Tao Pu, Leonardo; Koay, Doreen; Burt, Alastair (2016). "Sessile serrated adenoma/polyps: Where are we at in 2016?". World Journal of Gastroenterology. 22 (34): 7754. doi:10.3748/wjg.v22.i34.7754. ISSN 1007-9327.
  6. ↑ Kahi, Charles J.; Vemulapalli, Krishna C.; Snover, Dale C.; Abdel Jawad, Khaled H.; Cummings, Oscar W.; Rex, Douglas K. (2015). "Findings in the Distal Colorectum Are Not Associated With Proximal Advanced Serrated Lesions". Clinical Gastroenterology and Hepatology. 13 (2): 345–351. doi:10.1016/j.cgh.2014.07.044. ISSN 1542-3565.
  7. ↑ "StatPearls". 2018. PMID 29262150.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ Giacosa A, Frascio F, Munizzi F (2004). "Epidemiology of colorectal polyps". Tech Coloproctol. 8 Suppl 2: s243–7. doi:10.1007/s10151-004-0169-y. PMID 15666099.
  12. ↑ 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.
  13. ↑ Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD (2002). "Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential?". Cancer Epidemiol. Biomarkers Prev. 11 (10 Pt 1): 1012–8. PMID 12376501.
  14. ↑ Bonnington, Stewart N (2016). "Surveillance of colonic polyps: Are we getting it right?". World Journal of Gastroenterology. 22 (6): 1925. doi:10.3748/wjg.v22.i6.1925. ISSN 1007-9327.
  15. ↑ Bettington, Mark; Walker, Neal; Clouston, Andrew; Brown, Ian; Leggett, Barbara; Whitehall, Vicki (2013). "The serrated pathway to colorectal carcinoma: current concepts and challenges". Histopathology. 62 (3): 367–386. doi:10.1111/his.12055. ISSN 0309-0167.
  16. ↑ Johnson, David H.; Kisiel, John B.; Burger, Kelli N.; Mahoney, Douglas W.; Devens, Mary E.; Ahlquist, David A.; Sweetser, Seth (2017). "Multitarget stool DNA test: clinical performance and impact on yield and quality of colonoscopy for colorectal cancer screening". Gastrointestinal Endoscopy. 85 (3): 657–665.e1. doi:10.1016/j.gie.2016.11.012. ISSN 0016-5107.
  17. ↑ Villous adenoma. Wikipedia. https://en.wikipedia.org/wiki/Villous_adenoma Accessed on May 3, 2016
  18. ↑ Dehmer SP, Maciosek MV, Flottemesch TJ, LaFrance AB, Whitlock EP (2016). "Aspirin for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: A Decision Analysis for the U.S. Preventive Services Task Force". Ann. Intern. Med. 164 (12): 777–86. doi:10.7326/M15-2129. PMID 27064573.
  19. ↑ Winawer, Sidney J. (2015). "The History of Colorectal Cancer Screening: A Personal Perspective". Digestive Diseases and Sciences. 60 (3): 596–608. doi:10.1007/s10620-014-3466-y. ISSN 0163-2116.
  20. ↑ Rameshshanker, R.; Wilson, Ana (2016). "Electronic Imaging in Colonoscopy: Clinical Applications and Future Prospects". Current Treatment Options in Gastroenterology. 14 (1): 140–151. doi:10.1007/s11938-016-0075-1. ISSN 1092-8472.
  21. ↑ Lieberman DA, Rex DK, Winawer SJ, Giardiello FM, Johnson DA, Levin TR (2012). "Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer". Gastroenterology. 143 (3): 844–857. doi:10.1053/j.gastro.2012.06.001. PMID 22763141.
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