Updated: Dec 15, 2009
Colonic polyps are slow-growing overgrowths of the colonic mucosa that carry a small risk (<1%) of becoming malignant. However, because colonic polyps are highly prevalent in the general population (especially with increasing age), they confer an important predisposition to colon cancer and are therefore removed when detected.
Patients with isolated colonic polyps are usually asymptomatic but can experience overt or occult colonic bleeding. Colonic polyps can occur as part of inherited polyposis syndromes in which their number is greater and the risk for malignant progression is much greater compared to the risk with isolated colonic polyps.
In the context of clinical studies of chemoprevention, efforts are being directed at suppressing colonic polyp formation (eg, by use of sulindac) and/or at preventing their progression to colon cancer (eg, by use of aspirin).
Colonic polyps, or adenomas, are benign epithelial neoplasms that arise from the epithelial cells lining the colon. Colonic polyps are traditionally divided into 3 groups, as follows: hyperplastic polyps, adenomas, and polyposis syndromes.
Hyperplastic polyps
Hyperplastic polyps comprise about 90% of all polyps and are benign protrusions. They are usually less than 0.5 cm in diameter. Hyperplastic polyps most commonly occur in the rectosigmoid region during adulthood.
Thought previously to be entirely clinically insignificant, hyperplastic polyps are now recognized to possess some malignant potential in the setting of hyperplastic polyposis syndrome. Patients who are affected have an occurrence of hyperplastic polyps proximal to the sigmoid colon, with (1) 2 or more that are greater than 10 mm in diameter, (2) a total of more than 30 polyps, or (3) a first-degree relative with the syndrome. The polyps in this syndrome may have adenomatous components; display a serrated, saw-tooth surface epithelium; and harbor methylation of specific target genes, including mismatch repair genes.
Adenomas
Adenomas comprise approximately 10% of polyps. Most polyps (approximately 90%) are small, usually less than 1 cm in diameter, and have a small potential for malignancy. The remaining 10% of adenomas are larger than 1 cm and approach a 10% chance of containing invasive cancer.
Adenomas are traditionally divided by histology into 3 types, as follows: tubular, tubulovillous, and villous. Tubular adenomas are the most common of the 3 types and can be found anywhere in the colon. Villous adenomas most commonly occur in the rectal area; tend to be larger than the other two types; and tend to be nonpedunculated, velvety, or cauliflowerlike in appearance. Villous adenomas are associated with the highest morbidity and mortality rates of all polyps. They can cause hypersecretory syndromes characterized by hypokalemia and profuse mucous discharge and can harbor carcinoma in situ or invasive carcinoma more frequently than other adenomas.
Thus, the risk of progression to carcinoma is related to both the size and the histology of the adenoma. Adenomas that are greater than 1 cm, contain a substantial (>25%) villous component, or have high-grade dysplasia are commonly referred to as advanced neoplasms and carry an increased cancer risk.
The shape or gross structure of the polyp is also clinically significant. Those polyps with a stalk are called pedunculated. Those polyps without a stalk are called sessile. Sessile polyps are more concerning than large pedunculated polyps for two reasons. First, the pathway for migration of invasive cells from the tumor into submucosal and more distant structures is shorter. Second, the complete endoscopic removal is more challenging and more difficult to ascertain.
Some premalignant neoplasia is now recognized to be flat, rather than protuberant. Such nonpolypoid neoplasia is more common in the setting of chronic colitis and may be detected more readily by nontraditional endoscopic imaging methods, such as narrow-band width imaging or mucosal staining.
Polyposis syndromes
Polyposis syndromes are hereditary conditions that include familial adenomatous polyposis (FAP), hereditary nonpolyposis (a misnomer) colorectal cancer (HNPCC)/Lynch syndrome, Gardner syndrome, Turcot syndrome, Peutz-Jeghers syndrome, Cowden disease, familial juvenile polyposis, and hyperplastic polyposis.
Progress has been made in understanding some of the genetic factors contributing to the development of these syndromes. Some of the syndromes have extraintestinal features that help differentiate one syndrome from the other. For example, FAP is best understood in terms of the genetic basis and subsequent pathological and genetic events leading to carcinoma.
Two other types of benign polyps are hamartomatous polyps, which contain a mixture of normal tissues, and inflammatory polyps, which contain an inflammatory epithelial reaction and are typically found in the context of colitis.
Population and autopsy studies suggest that about 30% of middle-aged or elderly individuals have colonic polyps. In comparison, the incidence of FAP in the United States is 1 case for every 6580-8300 persons.
Accurate comparison of colonic polyp incidence and prevalence among countries is difficult because of differences in the methods used for detection. Colonic polyp prevalence in patients older than 60 years appears to vary substantially within and among countries, but it appears to be greater than 10% in most areas.
Untreated, colonic polyps can and do progress to carcinoma over several years. Morbidity from colonic polyps is related to complications, such as bleeding, diarrhea, intestinal obstruction, and progression to cancer. Bleeding can be frank hematochezia but is often chronic and goes unnoticed by the patient. If uncompensated, intestinal blood loss can cause anemia, typically due to iron deficiency.
A study by Stryker et al suggests that the risk of cancer development from sporadic 1-cm colonic polyps is 8% at 10 years and 24% at 20 years.[1 ]The risk for cancer development depends on the size of the polyp, villous histology, and its association with polyposis syndromes. In FAP, cancer inevitably develops 10-20 years after the initial appearance of colonic polyps.
Race per se is not a major risk factor for colonic polyps. However, studies indicate that blacks have a somewhat higher incidence and an earlier onset of colorectal carcinoma. An American Gastroenterological Association task force recommended beginning colorectal cancer screening in blacks at age 45 years, rather than the standard age of 50 years.
Males may have a modestly higher colonic polyp incidence than females.
Colonic polyps are strongly associated with increasing age (typically after age 40 y), but they can occur early in patients with polyposis syndromes. For example, colonic polyps can be detected in adolescents with familial adenomatous polyposis or in patients aged 20-40 years with hereditary nonpolyposis colorectal cancer (HNPCC).
Familial Adenomatous Polyposis
Gardner Syndrome
Inflammatory Bowel Disease
Peutz-Jeghers Syndrome
The differential varies, depending on the age of the patient and the presenting symptoms. A family history of polyposis is very significant because it raises the possibility of an inherited susceptibility, such as FAP or other polyposis syndromes. The differential diagnosis can be broad if the patient presents with rectal bleeding or diarrhea.
Adenomatous polyps are of 3 different histological types, as follows: tubular, villous, and tubulovillous. Adenomatous polyps may show changes of dysplasia, which distinguish them from hyperplastic polyps. The most common benign polyp is hyperplastic.
Colonic polyps are typically benign. Colonic polyps that contain high-grade dysplasia or microinvasive cancer confined to the mucosa are often termed carcinoma in situ.
Some studies have demonstrated that medical treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) decreases the number and the size of colonic polyps. However, NSAIDs, such as sulindac, do not prevent cancer development. These drugs do not yet constitute established therapies or chemopreventives for colonic polyps.
One study suggests that aspirin may be beneficial in reducing the incidence of recurrent colonic polyps, particularly advanced colonic polyps in select patients with a high risk of colon cancer and an acceptably low risk of gastrointestinal bleeding or hemorrhagic stroke.[9 ]
A regular diet may be continued. The patient can consider calcium and folate supplements to decrease the risk of colonic polyp recurrence.
Activities may be maintained as tolerated.
No drug therapy is proven or recommended for colonic polyps. More studies are required to assess the potential use of NSAIDs in order to elucidate their mechanism of action in causing colonic polyp regression and to determine why they do not appear to prevent cancer development.
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colonic polyps, colonic polyp, colon polyp, colon polyps, colon cancer, colon cancer polyp, colonoscopy, polyposis, HNPCC, colonoscopy polyp, hyperplastic polyps, familial adenomatous polyposis, Gardner syndrome, Turcot syndrome, Peutz-Jeghers syndrome, Cowden disease, familial juvenile polyposis, hereditary nonpolyposis colorectal cancer, polypectomy, colectomy
Gregory H Enders, MD, PhD, Member, Fox Chase Cancer Center
Gregory H Enders, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Gastroenterological Association, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.
Wafik S El-Deiry, MD, PhD, Professor of Medicine, Department of Hematology/Oncology; Co-Program Leader, Radiation Biology Program, Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine
Wafik S El-Deiry, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Clinical Investigation, and American Society of Gene Therapy
Disclosure: Nothing to disclose.
Manoop S Bhutani, MD, FACG, FACP, Professor, Department of Medicine, Division of Gastroenterology, Director, Center for Endoscopic Ultrasound, Co-Director, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch at Galveston
Manoop S Bhutani, MD, FACG, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
Research on colon neoplasia in the author's laboratory has been supported by NIH grant #R01DK64758.
Further ReadingClinical Guidelines
Quality indicators for colonoscopy. American College of Gastroenterology - Medical Specialty Society
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2006 Apr. 13 pages. NGC:004969
ASGE guideline: the role of endoscopy in the diagnosis, staging, and management of colorectal cancer.
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2005 Jan. 7 pages. NGC:004061
ACR Appropriateness Criteria® colorectal cancer screening.
American College of Radiology - Medical Specialty Society. 1998 (revised 2006). 7 pages. NGC:005544
Clinical trials
Calcium/Vitamin D, Biomarkers,& Colon Polyp Prevention (PPS4B)
Discard:Characterisation of Colonic Polyps in Vivo (DISCARD)
Confocal Probe-Based Endoscopic Imaging, Colorectal Cancer, Gastrointestinal (GI) Pathologies (ASGE-FNDT-1)
A Prospective, Single Blinded Study for Predicting Colon Polyp Histology With Narrow Band Imaging (NBI)
Related eMedicine topics
Intestinal Polyposis Syndromes
Familial Adenomatous Polyposis
Colorectal Tumors
Colonoscopy
Colon, Polyps
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