Villous adenoma

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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.

Classification

Gastrointestinal adenomas may be classified into 3 subtypes according to their histological appearance:

• Tubular
• Tubulovillous
• Villous

Villous adenoma can be classified into 4 types according to the gross appearance:

• 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 colonic poylp.
• The pathogenesis of villous adenoma is characterized by overgrowth of epithelial tissue with glandular characteristics.
• 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.
  • 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 .
  • These adenomas have a significant risk of metasstasis 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 suppresor genes.
• 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:
  • K-ras oncogene
  • Tumor suppresor p53 gene
  • APC gene on 5 chromosome associated with familial automatosis polyposis syndrome and Gardner syndome
  • STK11 (LBK1) gene, located on chromosome 19 associated with Peutz-Jeghers syndrome.
  • 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 cells and increased prostaglandin E2 are responsible for the diarrhea.

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 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: 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. 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. Other diagnostic studies Colonoscopy is the diagnostic modality of choice for villous adenoma. On colonoscopy, characteristic findings of villous adenoma include: 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. 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