Colonic Polyps



  • 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

  • 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)


  • 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
JPS imposes a higher risk of CRC, although juvenile polyps are not premalignant.

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