Intestinal Polypoid Adenomas 

  • Author: Alan BR Thomson, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jan 5, 2012
 

Background

The term intestinal polyp is used to describe any projection arising from flat mucosa into the intestinal lumen. Polyps can be broadly classified as neoplastic and nonneoplastic. Neoplastic polyps can be further classified as either adenomatous (premalignant) or malignant. Approximately 95% of all colorectal carcinomas are believed to arise from adenomas, a finding that underscores the importance of treatment and surveillance of adenomas of the gastrointestinal tract. See the images below.

Intestinal polypoid adenomas. Endoscopic view of pIntestinal polypoid adenomas. Endoscopic view of pedunculated polyp. Intestinal polypoid adenomas. Endoscopic view of sIntestinal polypoid adenomas. Endoscopic view of sessile polyp.

Adenomas represent approximately 60% of all polyps removed during colonoscopic examination of the colon. The cancer risk of adenomas is related to their macroscopic appearance (ie, size, attachment, location) as well as their microscopic architecture and degree of dysplasia. These descriptors are used clinically to predict the malignant potential of a polyp and to guide both treatment and future surveillance intervals.

Risk factors

  • Screening for premalignant adenomatous polyps has the potential of preventing advanced colorectal carcinoma (CRC). Colorectal adenomatous polyps are therefore targets for intervention, and they may also represent biomarkers for CRC risk.
  • Colonoscopic screening for adenomatous polyps of the colon and their removal provide a decreased risk of rectal and distal colon cancer but not of proximal cancer. This is presumed to be due to "missed" right-sided polyps.
  • In the United States, CRC is the third most common cancer diagnosed among men and women, and the second leading cause of death from cancer. As part of any encounter with a patient, a physician should advise patients of the choices they have for a screening test to detect polyps and to prevent CRC.
  • Consensus guidelines from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology were published in 2008 for the early detection of CRC and adenomatous polyps (see Further Reading).
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Pathophysiology

The colonic mucosa is a self-renewing epithelium that is a very tightly regulated balance between cell proliferation at the base of a crypt, maturation as colonocytes migrate up the crypt, and extrusion of senescent and/or apoptotic cells from the upper crypt into the lumen. This entire process takes approximately 3-6 days.

Adenomatous cells are characterized by loss of normal growth control. They continue to proliferate as they reach the top of the crypt, and they are not extruded into the lumen. Instead, they multiply and eventually fold back into the surrounding normal mucosa, inducing a response in the mesenchymal tissue that helps shape the microscopic architecture of the adenoma. The rate of growth and progression of adenomas to cancer is variable, but, typically, this occurs in 5-10 years. Patients with heritable forms of the disease, such as familial adenomatous polyposis (FAP) or hereditary nonpolyposis colorectal cancer (HNPCC), can have a more rapid rate of adenoma formation and progression to cancer.

The larger the index polyp, the more likely there may already be a focus of cancer. Barium enema studies suggest that the risk of developing cancer at the polyp site is as follows: at 5 years, 2.5%; at 10 years, 8%; and at 20 years, 24%. These growth characteristics are used to base the formulation of recommendations for surveillance after the index polyp has been found. When one adenoma is found, over one third of colons will have at least one more adenoma. The risk of cancer is increased with the number of polyps.

The adenoma-carcinoma sequence is thought to be a genetically driven process characterized by the occurrence over time of successive cycles of somatic mutation and clonal expansion of cells that have acquired a survival advantage. The first mutation in this process often involves inactivating mutations of the adenomatous polyposis coli (APC) tumor suppressor gene (inherited mutations in the APC gene cause FAP, and somatic mutations in the APC gene occur in about 80% of sporadic adenomas). Additional and progressive mutations occur in cells of the adenoma, including activating mutations of the oncogenes (Ki-ras) and inactivating mutations of tumor suppressor genes (ie, TP53) and/or DNA repair genes (ie, MSH2, MLH1). Epigenetic silencing of tumor suppressor and DNA repair genes by methylation may also contribute to this molecular process.

Some of these individual mutations lead to clones of cells that have acquired a survival advantage over surrounding cells, leading to a clone of mutant cells. Subsequent cycles of mutation and clonal expansion ultimately lead to adenoma growth, increased severity of dysplasia, and, ultimately, acquisition of the invasive and metastatic characteristics of an adenocarcinoma.

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Epidemiology

Frequency

United States

Colonoscopic and autopsy series suggest an overall prevalence of adenomatous polyps of 40-50% by age 50-60 years. The prevalence of colonic adenomas increases with age and varies depending on the inherent risk of colorectal cancer in a given population.

International

Significant geographic variation occurs throughout the world. For example, 2 different ethnic groups from genetically homogeneous regions in Japan have as much as a 20% difference in the prevalence of adenomas in people aged 50 years.

Mortality/Morbidity

Except for the rare adenoma that causes a clinically significant hemorrhage or obstruction, morbidity and mortality are primarily related to the carcinoma that can arise from an adenoma. The National Polyp Study, a large multicenter trial, has demonstrated that detection and removal of adenomas can be expected to substantially decrease the incidence of colorectal cancer.

Race

Although substantial variations in adenoma risk occur among different populations, race itself does not appear to be an independent determinant of risk. Dietary and environmental factors may have a role in explaining some of the differences observed throughout the world; Hawaiian-Japanese men have a high prevalence of adenomas, whereas some Japanese men have low risk. Similarly, blacks in New Orleans have a high risk for adenomas, while South African rural blacks are at low risk for developing adenomas.

  • African American men and women have a higher risk of polyps larger than 9 mm.
  • African American men and women older than age 60 years are also more likely to have large polyps in the proximal rather than in the distal intestine, they may develop CRC at a younger age, and they have a higher mortality rate.
  • CRC is also seen more commonly in individuals with a family history of polyps or colon cancer, a personal history of colonic polyps or cancer, inflammatory bowel disease involving the colon, acromegaly, ureterosigmoidostomy, and Streptococcus bovis bacteremia.

Sex

Some studies suggest that adenoma prevalence can be up to 30% higher in men than in women.

Age

The prevalence of adenomas increases progressively with age. Adenomas are uncommon in people younger than 30 years unless associated with a significant family history or familial syndrome. Most studies suggest that sporadic adenoma prevalence begins to increase substantially in people aged 40-50 years and continues to increase through age 80 years.

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Contributor Information and Disclosures
Author

Alan BR Thomson, MD  Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Dennis J Ahnen, MD  Staff Physician, Denver VA Medical Center and Professor of Medicine, University of Colorado Denver School of Medicine

Dennis J Ahnen, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Gastroenterological Association, Crohns and Colitis Foundation of America, and Gastroenterology Research Group

Disclosure: EXACT Sciences travel expenses Review panel membership

Specialty Editor Board

Rajeev Vasudeva, MD, FACG  Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association

Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Douglas M Heuman, MD, FACP, FACG, AGAF  Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Alex J Mechaber, MD, FACP  Senior 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.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

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 & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthor, John Riopelle, DO, to the development and writing of this article.

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Intestinal polypoid adenomas. Endoscopic view of pedunculated polyp.
Intestinal polypoid adenomas. Endoscopic view of sessile polyp.
Intestinal polypoid adenomas. Tubular adenoma, low-power view. Courtesy of G. Warren, MD, Rose Medical Center, Denver, Colo.
Intestinal polypoid adenomas. Villous adenoma, low-power view. Courtesy of G. Warren, MD, Rose Medical Center, Denver, Colo.
Intestinal polypoid adenomas. High-power view of adenomatous polyp with low-grade dysplasia. Courtesy of G. Warren, MD, Rose Medical Center, Denver, Colo.
Intestinal polypoid adenomas. Villous adenoma with grade IV invasive carcinoma. Courtesy of G. Warren, Rose Medical Center, Denver, Colo.
 
 
 
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