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An intestinal polyp is any mass of tissue that arises from the bowel wall and protrudes into the lumen. Most are asymptomatic except for minor bleeding, which is usually occult. The main concern is malignant transformation; most colon cancers arise in a previously benign adenomatous polyp. Diagnosis is by endoscopy. Treatment is endoscopic removal.
(See also the American College of Gastroenterology's practice guidelines for diagnosis, treatment, and surveillance for patients with colorectal polyps.)
Polyps may be sessile or pedunculated and vary considerably in size. Incidence of polyps ranges from 7 to 50%; the higher figure includes very small polyps (usually hyperplastic polyps or adenomas) found at autopsy. Polyps, often multiple, occur most commonly in the rectum and sigmoid and decrease in frequency toward the cecum. Multiple polyps may represent familial adenomatous polyposis (see Tumors of the GI Tract: Familial Adenomatous Polyposis). About 25% of patients with cancer of the large bowel also have satellite adenomatous polyps.
Adenomatous (neoplastic) polyps are of greatest concern. Such lesions are classified histologically as tubular adenomas, tubulovillous adenomas (villoglandular polyps), or villous adenomas. The likelihood of cancer in an adenomatous polyp at the time of discovery is related to size, histologic type, and degree of dysplasia; a 1.5‑cm tubular adenoma has a 2% risk of containing a cancer vs a 35% risk in 3‑cm villous adenomas. Serrated adenomas, a somewhat more aggressive type of adenoma, may develop from hyperplastic polyps.
Nonadenomatous (nonneoplastic) polyps include hyperplastic polyps, hamartomas, juvenile polyps, pseudopolyps, lipomas, leiomyomas, and other rarer tumors. Juvenile polyps occur in children, typically outgrow their blood supply, and autoamputate some time during or after puberty. Treatment is required only for uncontrollable bleeding or intussusception. Inflammatory polyps and pseudopolyps occur in chronic ulcerative colitis and in Crohn's disease of the colon. Multiple juvenile polyps (but not sporadic ones) convey an increased cancer risk. The specific number of polyps resulting in increased risk is not known.
Symptoms and Signs
Most polyps are asymptomatic. Rectal bleeding, usually occult and rarely massive, is the most frequent complaint. Cramps, abdominal pain, or obstruction may occur with a large lesion. Rectal polyps may be palpable by digital examination. Occasionally, a polyp on a long pedicle may prolapse through the anus. Large villous adenomas may rarely cause watery diarrhea that may result in hypokalemia.
Diagnosis
Diagnosis is usually made by colonoscopy. Barium enema, particularly double-contrast examination, is effective, but colonoscopy is preferred because polyps also may be removed during that procedure. Because rectal polyps are often multiple and may coexist with cancer, complete colonoscopy to the cecum is mandatory even if a distal lesion is found by flexible sigmoidoscopy.
Treatment
Polyps should be removed completely with a snare or electrosurgical biopsy forceps during total colonoscopy; complete excision is particularly important for large villous adenomas, which have a high potential for cancer. If colonoscopic removal is unsuccessful, laparotomy should be done.
Subsequent treatment depends on the histology of the polyp. If dysplastic epithelium does not invade the muscularis mucosa, the line of resection in the polyp's stalk is clear, and the lesion is well differentiated, endoscopic excision and close endoscopic follow-up should suffice. Patients with deeper invasion, an unclear resection line, or a poorly differentiated lesion should have segmental resection of the colon. Because invasion through the muscularis mucosa provides access to lymphatics and increases the potential for lymph node metastasis, such patients should have further evaluation (as in colon cancer—see Tumors of the GI Tract: Colorectal Cancer).
The scheduling of follow-up examinations after polypectomy is controversial. Most authorities recommend total colonoscopy annually for 2 yr (or barium enema if total colonoscopy is impossible), with removal of newly discovered lesions. If 2 annual examinations are negative for new lesions, colonoscopy is recommended every 2 to 3 yr.
Prevention
Aspirin and COX-2 inhibitors may help prevent formation of new polyps in patients with polyps or colon cancer.
(See also the Cochrane review abstracts: dietary fibre, calcium supplementation, and aspirin and NSAIDs for the prevention of colorectal adenomas and carcinomas.)
Familial Adenomatous Polyposis
Familial adenomatous polyposis (FAP) is a hereditary disorder causing numerous colonic polyps and resulting in colon carcinoma by age 40. Patients are usually asymptomatic but may have heme-positive stool. Diagnosis is by colonoscopy and genetic testing. Treatment is colectomy.
FAP is an autosomal dominant disease in which ≥ 100 adenomatous polyps carpet the colon and rectum. The disorder occurs in 1 in 8,000 to 14,000 people. Polyps are present in 50% of patients by age 15, and 95% by 35. Cancer develops before age 40 in nearly all untreated patients.
Patients also can develop various extracolonic manifestations (previously termed Gardner's syndrome), both benign and malignant. Benign manifestations include desmoid tumors, osteomas of the skull or mandible, sebaceous cysts, and adenomas in other parts of the GI tract. Patients are at increased risk of cancer in the duodenum (5 to 11%), pancreas (2%), thyroid (2%), brain (medulloblastoma in < 1%), and liver (hepatoblastoma in 0.7% of children < 5).
Symptoms and Signs
Many patients are asymptomatic, but rectal bleeding, typically occult, occurs.
Diagnosis
Diagnosis is made by finding > 100 polyps on colonoscopy. Diagnosed patients should have genetic testing to identify the specific mutation, which should then be sought in 1st‑degree relatives. If genetic testing is unavailable, relatives should be screened with annual sigmoidoscopy beginning at age 12, reducing frequency with each decade. If no polyps are evident by age 50, screening frequency is then the same as for average-risk patients.
Children of parents with FAP should be screened for hepatoblastoma from birth to age 5 yr with annual serum fetoprotein levels and possibly liver ultrasound.
Treatment
Colectomy should be done at the time of diagnosis. Total proctocolectomy, either with ileostomy or mucosal proctectomy and ileoanal pouch, eliminates the risk of cancer. If subtotal colectomy (removal of most of the colon, leaving the rectum) with ileorectal anastomosis is done, the rectal remnant must be inspected every 3 to 6 mo; new polyps must be excised or fulgurated. Aspirin or coxibs may inhibit new polyp formation. If new ones appear too rapidly or prolifically to remove, excision of the rectum and permanent ileostomy are needed.
After colectomy, patients should have upper endoscopy every 6 mo to 4 yr, depending on the number of polyps (if any) in the stomach and duodenum. Annual physical examination of the thyroid, and possibly ultrasound, also is recommended.
Peutz-Jeghers Syndrome
Peutz-Jeghers syndrome is an autosomal dominant disease with multiple hamartomatous polyps in the stomach, small bowel, and colon along with distinctive pigmented skin lesions.
Patients are at a significantly increased risk of GI and non-GI cancers; possibly the genetic defect involves a tumor suppressor gene. GI cancers include those of the pancreas, small intestine, and colon. Non-GI cancers include those of the breast, lung, uterus, and ovaries.
The skin lesions are melanotic macules of the skin and mucous membranes, especially of the perioral region, lips and gums, hands, and feet. All but the buccal lesions tend to fade by puberty. Polyps may bleed and often cause obstruction or intussusception.
Diagnosis is suggested by the clinical picture. Genetic testing is not routinely available but should be considered. First-degree relatives should be evaluated and have routine surveillance for cancers, but there is no firm consensus on specific tests and intervals.
Colonic polyps larger than 1 cm typically are removed.
Last full review/revision December 2007 by Elliot M. Livstone, MD
Content last modified December 2007
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