Description

• 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.

Epidemiology

Colorectal polyps are more common in non-Caucasian men in Western countries.

Incidence
Incidence increases with age.

Prevalence

• 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

• Mucosal
  • Neoplastic
    • Adenomatous polyps (tubular >80%, villous 5–15%, tubulovillous 5–15%)
    • Serrated polyps
    • Sessile serrated polyps (SSPs) 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)

Genetics

• 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.

Risk Factors

• 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).

General Prevention

• 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:

• Adenomatous
  • FAP
    • Classic (CFAP), attenuated (AFAP)
  • MAP
  • FAP variants:
    • Gardner syndrome, Turcot syndrome
• Hamartomatous
  • Peutz-Jeghers syndrome (PJS), JPS, Cowden syndrome