Colonic polyps are abnormal colonic mucosal overgrowths. They are a common finding in people over the age of 50. In rare cases, they may be seen in younger individuals as part of hereditary polyposis syndromes (e.g., familial adenomatous polyposis, ). On macroscopic examination, colonic polyps are either pedunculated (with a stalk) or sessile (without a stalk). Histologically, colonic polyps are most commonly adenomas (∼ 70%), followed by hyperplastic polyps, and, rarely, serrated polyps and hamartomatous polyps. Colonic polyps may be benign or have malignant potential. Adenomas have the highest malignant potential (∼ 5%) and most colonic carcinomas arise from them (adenoma-carcinoma sequence). Most patients are asymptomatic, but they may present with altered bowel habits, blood/mucus in stool, and iron deficiency anemia. Colonoscopy is the diagnostic modality of choice since it allows for direct visualization of the polyps, biopsy, and therapeutic snare polypectomy (of pedunculated polyps) or endoscopic submucosal resection (of sessile polyps). Large polyps (> 2 cm) or malignant polyps require surgical resection.
- ∼ 30% of individuals > 50 years
- Incidence increases with age.
- Sex: ♂ > ♀
Epidemiological data refers to the US, unless otherwise specified.
Macroscopic classification of colonic polyps
|Histologic classification of colonic polyps |
|Histological type||Subtypes||Characteristics||Malignant potential|
|Inflammatory polyps (pseudopolyps)|| |
|Mucosal polyps|| |
|Hamartomatous polyps |
|Serrated polyps|| |
Sessile serrated polyps
Traditional serrated adenoma
|Adenomatous polyps|| |
Villous adenomas are villains because they have the highest malignant potential.
Hereditary polyposis syndrome
Familial adenomatous polyposis (FAP)
- Clinical features
- Flexible sigmoidoscopy/colonoscopy
- Genetic testing: Detection of germline mutations in the APC gene establishes the diagnosis.
- Treatment 
- Prognosis: The lifetime risk of colorectal cancer is 100% by 45 years of age.
Variants of FAP
- FAP and extracolonic bony and/or soft tissue tumors; (e.g., osteomas of the mandible or skull, desmoid tumors, sebaceous cysts, lipomas, fibromas)
- Dental abnormalities (e.g., supernumerary and/or impacted teeth) present in ∼ 30% of cases 
- Associated with congenital hypertrophy of the retinal pigment epithelium
- APC gene mutation with autosomal dominant inheritance
- The lifetime risk of developing colorectal cancer is 100%.
- Turcot syndrome
- Attenuated FAP
The Turban covers the head: Turcot syndrome is associated with malignant brain tumors.
MYH-associated polyposis 
- Etiology: autosomal recessive mutation in the MUTYH gene
- Prognosis: The lifetime risk of colorectal cancer is 80–90%.
Peutz-Jeghers syndrome 
- Etiology: autosomal dominant mutation of the STK11 gene on chromosome 19p13.3 → loss of tumor suppressor function → hyperactive serine‑threonine kinase
- Clinical features: ∼ 95% of patients have hyperpigmented macules; that typically affect the lips (perioral lentigines), buccal mucosa, genitals, palms, and soles
- Diagnostics: multiple hamartomatous polyps throughout the gastrointestinal tract on endoscopy
- Prognosis 
Juvenile polyposis syndrome (JPS) 
- Etiology: autosomal dominant with incomplete penetrance 
- Epidemiology: : onset within the first decade of life (most commonly affects children < 5 years of age)
- Clinical features: gastrointestinal bleeding and anemia
- Diagnostics: > 10 hamartomatous polyps throughout the gastrointestinal tract (e.g., colon, stomach, small bowel) on endoscopy
- Prognosis: increased lifetime risk of colorectal cancer (∼ 20%)
Cowden syndrome 
- Etiology: most commonly due to autosomal dominant mutations of the PTEN gene
- Clinical features
Cronkhite-Canada syndrome 
- Laboratory tests
- Colonoscopy (confirmatory test)
- Flexible sigmoidoscopy
Treatment depends on the etiology and nature of the polyp or polyps.
These recommendations are consistent with the US Multi-Society Task Force on Colorectal Cancer 2020 guidelines.