- Intraluminal colonic tissue growth; most commonly sporadic or part of polyposis syndromes
- Generally slow growing with low malignant potential; due to high prevalence in population; however, resection is generally recommended to eliminate risk.
- Size classification:
- Diminutive ≤5 mm, small 6 to 9 mm, large ≥10 mm
- Morphologic classification:
- Depressed, flat, sessile, or pedunculated
- Clinical significance:
- >95% of colonic adenocarcinomas arise from polyps.
Colorectal polyps are more common in non-Caucasian men in Western countries.
Incidence increases with age.
- 15–20% of all adults
- 30% of U.S. population aged >50 years
- 6% of children
- 12% of children with lower GI bleed
Etiology and Pathophysiology
- Adenomatous polyps (tubular >80%, villous 5–15%, tubulovillous 5–15%)
- Serrated polyps
- Sessile serrated polyps are common, more in proximal colon, with low malignant potential if no dysplasia and significant malignant potential if dysplastic.
- Traditional serrated adenoma is uncommon, more often noted in distal colon, with significant malignant potential.
- Nonneoplastic polyps (hyperplastic, juvenile polyps, hamartomas, inflammatory pseudopolyps)
- Hyperplastic polyps are very common, more in distal colon, with very low malignant potential.
- Juvenile polyps are common in childhood, benign hamartomas, more in rectosigmoid, and not premalignant.
- Submucosal (lipomas, lymphoid aggregates, carcinoids)
- Inactivation of tumor suppressor genes as adenomatous polyposis coli (APC) or mismatch repair genes (MLH1) causes polyps to grow into cancer.
- Familial adenomatous polyposis (FAP) is autosomal dominant. By age 40 years, almost all patients develop colorectal cancer (CRC).
- MUTYH-associated polyposis (MAP) is autosomal recessive caused by biallelic mutations in MUTYH gene.
- Juvenile polyposis syndrome (JPS) is autosomal dominant. 50–60% of patients have a mutation in the SMAD4 or BMPR1A gene. By age 35 years, 20% of patients develop CRC.
- Family history of intestinal polyposis, polyps, or CRC
- Advancing age; male
- High-fat, low-fiber diet; tobacco use
- Excessive alcohol intake: more than eight drinks a week
- Inflammatory bowel disease is associated with a decreased prevalence of colon polyps (but with higher risk of colon cancer).
- Low-fat, high-fiber diet
- Avoid smoking.
- Decrease alcohol intake.
- Use of NSAIDs and calcium is associated with decreased incidence and recurrence of polyps.
- No lower rates of CRC with azathioprine, 6-mercaptopurine, folate, calcium, multivitamins, or statins
Commonly Associated Conditions
Hereditary polyposis syndromes:
- Classic (CFAP)
- Attenuated (AFAP)
- FAP variants:
- Gardner syndrome
- Turcot syndrome
- Peutz-Jeghers syndrome (PJS)
- Familial juvenile polyposis
- Cowden syndrome
JPS imposes a higher risk of CRC, although juvenile polyps are not premalignant.
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