Synonyms and related keywords
papillary adenoma, malignancy, tubular adenoma, tubulovillous adenoma, tubulo-villous adenoma, colonoscopy, adenocarcinomas, rectal cancer, colon cancer, colonic villous adenomas, adenomatous polyps
Author: Alnoor Ramji, MD, Fellow, Department of Medicine, Division of Gastroenterology, University of British Columbia, Vancouver, Canada
Coauthor(s): Eric M Yoshida, MD, MHSc, FRCPC, FACP, Program Director of Adult Gastroenterology Training Program, Assistant Professor, Department of Medicine, Division of Gastroenterology, University of British Columbia
Alnoor Ramji, MD, is a member of the following medical societies: British Columbia Medical Association, Canadian Association of Gastroenterology, and Canadian Society of Internal Medicine
Editor(s): Manoop S Bhutani, MD, Associate Professor of Medicine, Division of Gastroenterology, University of Texas Medical Branch at Galveston; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine; Alex J Mechaber, MD, FACP, Director of Clinical Skills Program, Assistant Professor, Department of Internal Medicine, Division of General Internal Medicine, University of Miami School of Medicine; and Julian Katz, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, MCP Hahnemann University
Background: Adenomatous polyps are, by definition, neoplastic. Although benign, they are the direct precursors of adenocarcinomas and follow a predictable cancerous temporal course unless interrupted by treatment. They can be either pedunculated or sessile. Adenomas are divided into 3 subtypes based on histologic criteria, (1) tubular, (2) tubulovillous, and (3) villous. According to World Health Organization (WHO) criteria, villous adenomas are composed of greater than 80% villous architecture. Tubular adenomas are encountered most frequently (80-86%). Tubulovillous adenomas are encountered less frequently (8-16%), and villous adenomas are encountered least frequently (5%).
Villous adenomas are associated more often with larger adenomas and more severe degrees of dysplasia. These adenomas occur more frequently in the rectum and rectosigmoid, although they may occur anywhere in the colon. They generally are sessile structures that appear as velvety or cauliflowerlike projections. Although rare, villous adenomas of the duodenum and small bowel, particularly at the ampulla, can occur. Villous adenomas are of concern primarily because of the risk of malignant transformation (approximately 15-25% overall but higher once >2 cm).
The primary focus of this article is colonic villous adenomas. Where appropriate, certain aspects of small bowel villous adenomas are addressed.
Pathophysiology: Adenomas are believed to have an abnormal process of cell proliferation and apoptosis. The proliferative component is not confined to the crypt base and accumulates onto the surface and infolds downward. In villous adenomas, mesenchymal proliferation results in longer projections and larger polyps.
Clinical, autopsical, and epidemiological studies provide evidence of adenoma-to-carcinoma progression. The mean age of adenoma diagnosis is 10 years earlier than with carcinoma, and progression to carcinoma takes a minimum of 4 years.
Molecular genetic studies also describe an adenoma-to-carcinoma sequence through accumulation of lesions in a variety of genes, with activation of oncogenes and inactivation of tumor suppressor genes. The K-ras oncogene is described in 9% of small adenomas, 58% of adenomas larger than 1 cm, and 46% of colorectal carcinomas. Inactivation of tumor suppressor genes on arms 5q, 18q, and 17p are thought to be essential in tumorigenesis. The APC gene, on 5q, has an important role in adenoma formation. The gene is mutated in 30-60% of persons with sporadic adenomas and adenocarcinomas. Mutation on the TP53 gene, on 17p, results in malignant transformation of adenomas. The loss of TP53 is infrequent in patients with adenomas but occurs in more than 75% of patients with adenocarcinomas. The loss of the DCC (deleted in colon cancer) gene, on 18q, occurs in 50% of patients with adenomas and 70% of patients with carcinomas.
- In the US: The prevalence of adenomas closely parallels the risk of colorectal cancer in a region. Adenomas are found in 30-40% of persons aged 60 years or older; in some areas, as many as 50% have adenomas.
- Internationally: In regions of low risk for colon carcinoma (eg, Costa Rica, Columbia), prevalence rates are 12%. This rate increases drastically in high-risk regions (eg, United States, Canada, western Europe, Argentina, New Zealand, Australia) to 30-40%. In some areas, rates approach 50%.
Mortality/Morbidity: The immediate risks of adenomas include hemorrhage, obstruction with intussusception, and, possibly, torsion. However, the main concern is malignant progression of the villous adenoma. Studies have defined the risk of progression of adenomas to adenocarcinoma.
- Precolonoscopy studies show the cumulative risk for carcinoma from polyps larger than 1 cm to be 4%, 14%, and 37% with 5, 10, and 20 years of follow-up, respectively. The risk for persons with carcinoma at sites other than the reference polyp is 4 times greater than that of the general population. The likelihood that an adenoma contains villous tissue, high-grade dysplasia, or invasive carcinoma is proportional to its size.
- Using complete colonoscopies, the National Polyp Study (NPS) prospectively followed 1418 patients diagnosed with 1 or more adenomas. An incidence reduction rate of 76-90% of colorectal cancers occurred, with only 10-24% of cancers that would be predicted from a reference population. This study found that the only independent predictive factors for progression from adenoma to adenocarcinoma were adenoma size and villous histology. The NPS study defined advanced polyps as larger than 1 cm or as those containing villous tissue or high-grade dysplasia.
- Overall, villous adenomas have a malignant risk of 15-25%. The risk of adenocarcinoma approaches 40% in villous adenomas larger than 4 cm in diameter. Patients with a rectosigmoid adenoma larger than 1 cm (or villous histology) had a 3.6-fold risk of developing adenocarcinoma compared to the general population. Villous adenomas of the ampulla of Vater contain carcinoma in 30-50% of cases, and carcinoma is found in 20-25% of duodenal villous adenomas.
Race: Race is not an independent factor for adenoma prevalence, although region is considered to be a factor.
- This is well described in the Hawaiian-Japanese population, which has much higher rates of adenoma than the Japanese population.
- A similar situation exists with black Americans (higher rates) and black in South Africans.
Sex: Generally, adenoma risk is independent of sex, although some authorities suggest a slight male predominance.
Age: The prevalence and distribution of adenomas varies with patient age.
- The prevalence of adenomas increases with age. The prevalence of polyps at 50 years is 30%, at 60 years is 40-50%, and at 70 years is 50-65%.
- Distribution of polyps differs with age. In patients aged 55 years or younger, 75% of polyps 10 mm or larger were located distally. In patients aged 65 years and older, 50% of polyps 10 mm or larger were located proximally.
History: Note that the vast majority of patients are asymptomatic and have unremarkable laboratory findings. Any nonspecific intestinal symptoms are more likely to be coincidental.
- The most common presenting symptom is occult/overt bleeding (hematochezia) with an anemia, which may be microcytic. Polyps may bleed only intermittently into the stromal component, thus accounting for inconsistent findings.
- Nonspecific symptoms include diarrhea, constipation, and flatulence. A change in stool caliber (ie, the classic pencil-thin stools), although still described in older textbooks, is an entirely nonspecific and unreliable symptom. Pencil-thin stools, if truly present, would be secondary to large distal adenomas or frank carcinomas.
- When intense cramping occurs, torsion or episodic intussusception due to larger adenomas may be considered.
- Villous adenomas rarely cause a secretory diarrhea syndrome. The tumor usually is located at the rectosigmoid or rectum and often is 3-4 cm in diameter. Stool volumes of 350-3000 mL are reported and may cause hypovolemia and metabolic imbalances.
- Patients may have a family history of polyps and colon cancer.
- Patients with villous adenomas of the ampulla usually present with intermittent or progressive jaundice, abdominal pain, intestinal hemorrhage, or pancreatitis.
- Patients often have no findings on bedside physical examination.
- Occasionally, a palpable mass is present upon digital rectal examination.
- Jaundice may be present with villous adenoma of the ampulla.
- Genetic factors: From the NPS data, relatives of patients with polyps have an increased risk of carcinoma. This includes siblings of patients with adenomas detected prior to age 60 years or siblings of patients with adenomas detected at any age if either parent has colorectal cancer. Offer these patients screening colonoscopy every 5 years after age 40 years.
- Lifestyle and diet: Foods and vitamins that have a protective effect against adenomas include dietary fiber, plant foods, carbohydrates, and folate supplementation. Excess fat and alcohol are positively correlated with adenoma risk. A strong association exists between cigarette smoking and adenoma size. Supplemental vitamins C and E are not considered protective.
- Acromegaly: Patients with acromegaly have an increased risk of adenomas and colon cancer. Prevalence rates of 14-35% for adenomas are reported. The mechanism for increased risk is not known.
- Streptococcus bovis bacteremia: This causes an increased risk of adenomas, carcinomas, and, possibly, familial adenomatous polyposis (FAP). These patients should undergo colonoscopy. Patients with endocarditis from Streptococcus agalactiae infection are reported to have an increased risk of rectal villous adenoma and should be evaluated.
- Atherosclerosis and cholesterol: Autopsy studies report a positive correlation between the degree of atherosclerosis and adenoma size, dysplasia, and multiplicity.
- Uterosigmoidostomy sites: Patients who undergo urinary diversion procedures are at increased risk of developing polyps or carcinomas at uterosigmoidostomy sites as many as 38 years later. Prevalence rates of 29% are reported.
- Inflammatory bowel disease (IBD): In patients with IBD who develop carcinomas, 50% of the lesions are found to be juxtaposing serrated or villous adenomas. These possibly are the lesions from which the carcinomas originate. However, a dysplasia-associated lesion or mass is reported to be the premalignant lesion of adenocarcinoma in ulcerative colitis, in which the adenoma-carcinoma sequence is not preserved.
- Other conditions: Historically, some conditions have been thought to be correlated with increased incidence of polyps. These conditions include acrochordons (skin tags), breast cancer, and cholecystectomy, for which no evidence exists of an increased risk for adenoma.
Familial Adenomatous Polyposis
Other Problems to be Considered:
Granular cell tumor
Solitary rectal ulcer
- Complete blood cell count: A low hemoglobin level and a classic low mean cell volume (MCV) suggest iron deficiency anemia, but these values can be within reference ranges or can be considered nonspecific findings if small polyps are present.
- Iron studies: Obtain ferritin levels, serum iron levels, and transferrin saturation values. Patients with iron-deficiency anemia have low ferritin and serum iron levels and low transferrin saturation.
- Fecal occult blood testing (FOBT): Only 20-40% of patients with adenomas have positive test findings, usually resulting from distal and larger polyps.
- Genetic studies: These are not performed routinely in the evaluation of sporadic polyps.
- Double-contrast barium enema
- Double-contrast barium enemas have a higher sensitivity compared to single-contrast barium enemas. Sensitivity increases with polyp size.
- A well-performed air-contrast barium enema has a sensitivity of 85-90% for polyps larger than 1 cm and 61% for polyps smaller than 1 cm. A false-positive rate of 5-10% is found because of improper cleaning of the bowel. Diverticulosis or redundant bowel can result in a false-negative rate of 10%, especially in the rectosigmoid. The accuracy of the procedure also can have an element of operator-dependence.
- For all structural evaluations of the large bowel, use sigmoidoscopy with a barium enema.
- Computed tomographic colonography (virtual colonoscopy)
- Computed tomographic colonography is a newer method that is not as sensitive as colonoscopy, although it has the advantage of being less invasive. This scanning still requires bowel preparation.
- When compared to colonoscopy, computed tomographic colonography was able to identify all polyps larger than 1 cm, 71% of polyps of 0.5-0.9 cm, and only 28% of polyps smaller than 0.5 cm. More studies comparing colonoscopy with virtual colonoscopy are needed before making firm recommendations regarding the role of virtual colonoscopy in screening for colon polyps.
- Upper GI series and small bowel follow-through: These studies detect small bowel adenomas and can help investigate the small bowel for polypoid lesions beyond the reach of the conventional upper endoscope. They also help detect mass abnormality in 50-80% of patients and can help successfully define neoplasms in 30-44% of patients.
Histologic Findings: Adenomatous epithelium has abnormal cellular differentiation with hypercellularity and variable amounts of mucin. The predominant cell type is columnar epithelium, and immature goblet cells may be observed. The dysplastic cells demonstrate elongated nuclei, are hyperchromatic, and have a picket-fence appearance.
Villous histology is characterized by glands arranged in long fingerlike fronds from the polyp surface down to the polyp stroma. Projections usually extend straight down with minimal or no branching.
Staging: Dysplasia is subdivided into mild, moderate, and severe categories.
- Mild dysplasia is characterized by uniform loss of mucin and hyperchromatic and elongated cells. Glands appear branched and budding.
- Moderate dysplasia has more prominent nucleoli with increased crowding of cells.
- In severe dysplasia, increased nuclear pleomorphism, prominent and numerous nucleoli, and increased nuclear-to-cytoplasmic ratio occur. With continued cell proliferation, glands appear to form within glands, with a disordered cribriform appearance, and appear as carcinoma in situ.
- A full colonoscopy is the accepted procedure of choice in North America for screening or investigation of possible adenomas. If possible, remove all polyps at endoscopy. Send polyps to a pathologist to assess for histological type, grade of dysplasia, and presence of carcinoma. Record the gross morphology, location, and size of each polyp.
- Perform a full colonoscopy if sigmoidoscopy reveals an adenoma. Of patients with rectosigmoid adenomas, 40-50% have additional proximal polyps. From the NPS data, patients with left-sided adenomas had a 2.9-fold risk of also having right-sided polyps compared to patients with no left-sided polyps. Patients with only a hyperplastic polyp in the rectosigmoid do not require full colonoscopy.
- Cautery snare is recommended for removal of larger polyps. For large sessile polyps, for which the risk of perforation is higher, injection of 1 mL or more of saline into the submucosa directly under the polyp is a useful technique. This lifts the flat polyp away from the muscular layer, creating a stalklike effect. A couple of drops of methylene blue added to the saline also allows the operator to determine if a perforation has occurred in the muscle layer, which would be seen as a break in the layer. Smaller sessile polyps should be removed or biopsied and ablated with hot-biopsy forceps or a minisnare.
- The role for nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors is unclear. No evidence indicates regression in patients who already have polyps who are treated with these agents, although NSAIDS may have a role in primary prophylaxis.
- Surgical resection of a colorectal polyp may be required, especially if the polyp is larger than 2-3 cm and is sessile (as villous adenomas often are). Also, polyps encompassing 2 colonic folds often require surgical consideration. In such situations, the colonic wall can be marked with India ink for localization of the bowel segment at surgery.
- If benign, duodenal villous adenomas can be treated by local transduodenal resection, although recurrence is common and may be malignant. Consider pancreaticoduodenectomy for duodenal malignant villous adenomas and for villous tumors of the ampulla of Vater.
- A competent endoscopist should supervise care and follow-up.
- Consultation with a surgeon may be required for resection of the polyp.
- Dietary recommendations have been established to prevent colorectal cancer. Given the evidence for the adenoma-to-carcinoma sequence, these recommendations likely also apply to adenomas.
- Fat intake: Limit total fat to 25-30% of energy intake. A fatty diet may increase biliary sterols, which are damaging.
- Fruit and fiber intake: Increase fruit and fiber intake to 5 servings daily. Increased fiber dilutes luminal contents and decreases the contact between carcinogenic substances and the lumen. Fruits and vegetables also contain minerals and vitamins that may impede carcinogenesis.
- Fiber intake: Ingest 20-30 g of fiber daily. In addition to the benefits of increased fruit and fiber intake, fiber may inhibit some harmful bacteria and prevent damaging effects of bile acids.
- Maintain normal body weight.
- Exercise daily. Exercise helps decrease transit time and, therefore, the contact of harmful substances with the lumen.
- Avoid smoking and excessive consumption of alcohol.
The literature supports the use of NSAIDs in FAP syndrome, with regression of polyps already present. It has been demonstrated that COX-2 is up-regulated 2-50 times in most (85-90%) adenocarcinomas. The role for NSAIDs (including the newer COX-2 inhibitors) in nonfamilial adenomatous lesions is unclear. For sporadic polyps, NSAID use has not been proven to cause regression in already developed polyps, although evidence suggests a decreased incidence of polyps in persons already taking NSAIDs. Therefore, a potential role exists for NSAIDs as primary prophylaxis.
Drug Category: Nonsteroidal anti-inflammatory drugs -- Mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions, also may exist.
|Sulindac (Clinoril) -- Sulfoxide NSAID that is metabolized to the anti-inflammatory sulfide metabolite and a sulfone metabolite. Sulfide metabolite is now known to have apoptotic activity on colonic epithelial cells and is presumed to be responsible for regression of adenomatous polyps. Primary route of excretion is via urine as both sulindac and its sulfone metabolite. |
|150 mg PO bid; not to exceed 400 mg/d |
|Not established |
|Documented hypersensitivity; GI tract bleed; renal insufficiency |
|Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
|C - Safety for use during pregnancy has not been established. |
|Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs; caution in anticoagulation defects or patients who are receiving anticoagulant therapy|
|Celecoxib (Celebrex) -- Mechanism of action is through inhibition of prostaglandin synthesis, primarily of COX-2. Inhibition of COX-1 may contribute to NSAID GI tract toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. COX-2 is overexpressed in colonic adenomas. Inhibition of COX-2 is believed to cause adenoma regression. Eliminated predominantly by hepatic metabolism via cytochrome P-450 2C9. |
|400 mg PO bid |
|Not established |
|Documented hypersensitivity |
|Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations |
|B - Usually safe but benefits must outweigh the risks. |
|Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, severe heart failure, and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction or in abnormal liver lab results|
Further Outpatient Care:
- Surveillance colonoscopy (after initial colonoscopy and clearing of polyps)
- First follow-up colonoscopy
- The first follow-up colonoscopy should be performed within 3 years for most patients.
- If patients have multiple or villous adenomas, colonoscopy may be required earlier than 3 years.
- In patients at low risk (2 or fewer small [<0.5 cm] tubular adenomas), repeat colonoscopy at 5 years.
- Subsequent follow-up
- If the first follow-up results are negative, the second colonoscopy can be performed 5 years later.
- Surveillance can be discontinued, depending on comorbid conditions and age.
- Screening for polyps and adenocarcinoma: FOBT and sigmoidoscopy have been studied as screening tools.
- The use of annual FOBT has reduced colorectal cancer mortality rates by 15-43%. A major limitation is the low sensitivity for precancerous polyps.
- Cohort and case control studies have shown a 60-85% decrease in distal colorectal cancer rates when flexible sigmoidoscopy is used. A limitation of sigmoidoscopy is its reach; it misses approximately 40% of proximally located cancers.
- Current screening recommendations for the asymptomatic average-risk population (US Preventive Services Task Force) are as follows:
- Begin screening at age 50 years.
- In North America, a full colonoscopy is the primary accepted procedure of choice for the screening of adenomas.
- Perform colonoscopy for a positive test result.
- Individualize for age and comorbidity.
- Different guidelines exist for patients at higher risk of colorectal cancer. These include patients with FAP syndromes, Lynch syndromes, and familial risk for sporadic cancers.
- See Diet and Activity.
- Bowel torsion
- Malignant transformation
- Transformation to malignancy is a primary consideration in villous adenomas.
- Villous adenomas have a malignant risk of 15-25%. The risk of adenocarcinoma approaches 40% in villous adenomas larger than 4 cm in diameter.
- Villous adenomas of the ampulla of Vater contain carcinoma in 30-50% of patients.
- Carcinoma is found in 20-25% of duodenal villous adenomas.
- Emphasize the importance of continued surveillance once polyps are identified.
- Provide screening information for family members when appropriate.
- Failure to discuss the material risks of endoscopy with the patient and failure to instruct patients to schedule follow-up if they suspect complications
- Failure to carefully document polyp morphology, size, and location at endoscopy
- Failure to send all biopsies for identification of tissue histology
- Failure to perform regular follow-up evaluations for patients with polyps and failure to discuss implications for family members when appropriate
Caption: Picture 1. Endoscopic view of a sessile polyp, which histology studies revealed to be a villous adenoma. Courtesy of H. Chaun, MD.
Caption: Picture 2. Endoscopic view of a sessile polyp histologically determined to be a villous adenoma. Courtesy of R. Enns, MD
Caption: Picture 3. Endoscopic view of injection of saline into the base of a sessile polyp histologically determined to be a villous adenoma. This enables an easier polypectomy. Courtesy of R. Enns, MD.
Caption: Picture 4. Polypectomy with a snare around a sessile polyp base (villous adenoma) injected with saline. Courtesy of R. Enns, MD
Caption: Picture 5. Histology of villous adenoma. Fingerlike projections stretching from the surface of a polyp downward with minimal branching. Courtesy of D. Owen, MD.
Caption: Picture 6. Histology of villous adenoma. Low-grade dysplasia with loss of mucin, prominent nucleoli, and hyperchromatic and elongated cells. Courtesy of D. Owen, MD.
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