AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Polyps are slow-growing overgrowths of the colonic mucosa that carry a small risk (<1%) of becoming malignant. However, because 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 polyps are usually asymptomatic but can experience overt or occult colonic bleeding. 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 polyps. In the context of clinical studies of chemoprevention, efforts are being directed at suppressing polyp formation (eg, by use of sulindac). Administration of sulindac or vitamins C or E is an experimental approach, and long-term benefit remains unsubstantiated.

Pathophysiology

Colonic polyps, or adenomas, are benign epithelial neoplasms that arise from the epithelial cells lining the colon. Polyps are traditionally divided into 3 groups.

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, these lesions are now recognized to possess some malignant potential in the setting of the hyperplastic polyposis syndrome. Patients who are affected have an occurrence of hyperplastic polyps proximal to the sigmoid colon, with 2 or more that are greater than 10 mm in diameter, a total of more than 30 polyps, or 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 (~90%) are small, usually less than 1.5 cm in diameter, and have a very small potential for malignancy. The remaining 10% of adenomas are larger than 1.5 cm and have about a 10% chance of containing invasive cancer. Adenomas are traditionally divided into 3 types: tubular, tubulovillous, and villous. Tubular adenomas are the most common of the 3 types and can be found anywhere in the colon. Those with a distinct stalk are termed pedunculated; those without a stalk are termed sessile.

The risk of progression to carcinoma is related to the size of the adenoma. Tubulovillous adenomas are most commonly found in the rectal area. The degree of villous component of these adenomas is correlated with the risk of progression to carcinoma.

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.

Polyposis syndromes

Polyposis syndromes are hereditary conditions that include familial adenomatous polyposis (FAP), 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. 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.

Frequency

United States

Population and autopsy studies suggest that about 30% of middle-aged or elderly individuals have colonic polyps. The incidence of FAP in the United States is 1 case for every 6580-8300 persons.

International

Accurate comparison of polyp incidence and prevalence among countries is difficult because of differences in the methods used for detection. 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.

Mortality/Morbidity

Untreated, polyps can and do progress to carcinoma over several years. Morbidity from 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 polyps is 8% at 10 years and 24% at 20 years. The risk for cancer development depends on the size of the polyp, villous histology, and its association with the polyposis syndromes. In FAP, cancer inevitably develops 10-15 years after initial appearance of polyps.

Race

Race per se is not a major risk factor for polyps. However, studies indicate that blacks have a somewhat higher incidence and an earlier onset of colorectal carcinoma. A recent American Gastroenterological Association task force recommended beginning colorectal cancer screening in blacks at age 45 years, rather than the standard age of 50 years.

Sex

Males may have a modestly higher polyp incidence than females.

Age

Polyps are strongly associated with increasing age but can occur early in patients with polyposis syndromes. For example, they can be detected in adolescents with familial adenomatous polyposis.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• History of present Illness
• • Most patients are asymptomatic.
  • In symptomatic patients, the most common presenting symptom is rectal bleeding. Other symptoms include diarrhea or constipation, often with decreased stool caliber.
  • Villous adenomas of the rectum and distal colon can occasionally manifest as a syndrome of severe diarrhea with massive fluid and electrolyte loss.
  • Chronic bleeding from polyps may cause iron deficiency anemia.
• Family history: Although colonic polyps are a disease of older individuals, a positive family history of polyposis should prompt referral for screening in younger individuals and, in some cases, at more frequent intervals. A common practice is to begin screening in a patient 5 years earlier than the age at which polyps were diagnosed in a first-degree relative.

Physical

• Distal rectal polyps can be detected by digital rectal examination. Otherwise, physical examination findings are typically normal.
• Occult blood in stools (detected by guaiac and antibody-based tests) may be found in a minority of patients.
• • Although nonspecific, this finding should prompt a colon evaluation in most patients.
  • Such evaluations have had similar yields of clinically significant findings whether the stool sample was obtained by digital rectal examination or was retrieved from spontaneously passed stools.

Causes

• Epidemiologic studies suggest that environmental causes contribute to differences in polyp incidence in geographically distinct populations, but the responsible factors have remained elusive.
• Differences in consumption of dietary fiber and antioxidants have been hypothesized to play a role in the development of polyps, but these proposals have not been substantiated in recent studies. There is limited, circumstantial evidence that consumption of meat, fat, and alcohol may be risk factors. Conversely, consumption of calcium and folate may confer a modest protective effect, particularly in patients with a history of polyps and low basal consumption levels.
• Genetics
• • A number of polyposis syndromes have been described. These can be associated with specific extraintestinal manifestations as well as extraintestinal tumors.
  • Identification and characterization of the genetic factors leading to the various syndromes is progressing.
  • At the genetic level, FAP is understood best. This is an autosomal dominant disorder caused by truncating mutations in the adenomatous polyposis coli (APC) gene.
  • Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant disorder caused by mutations in DNA mismatch repair proteins.
  • Cowden disease is associated with mutations in the pentaerythritol tetranitrate (PTEN) protein phophatase.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

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.

• Sporadic polyps associated with aging
• Benign adenoma/hyperplastic polyp
• Pseudopolyps associated with inflammation
• Juvenile polyposis
• Basal cell nevus syndrome (includes basal cell carcinomas and colonic hamartomatous polyps)
• Turcot syndrome (includes polyps, medulloblastoma, congenital hypertrophy of the retinal pigmented epithelium [CHRPE], and glioblastoma multiforme)
• Cowden syndrome (includes polyps, fibrocystic disease, breast cancer, and thyroid cancer)

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• No laboratory test can determine definitively whether a given patient has a colonic polyp. A stool occult blood test can detect a fraction (20-40%) of polyps that are greater than 10 mm in diameter but can also reflect other causes of gastrointestinal blood loss.
• A patient with a family history of FAP may inherit a mutation in the APC gene.
• • A blood test may detect this heterozygous state.
  • Because most APC mutations involve truncations of the protein, an in vitro protein truncation assay has been developed by Powell et al. This assay amplifies segments of APC messenger RNA (mRNA) and expresses the protein parts in vitro to readily detect the truncated products. A positive test finding only indicates susceptibility, not the actual presence of a polyp.
• Genetic testing of blood samples can also detect the majority of cases of hereditary nonpolyposis colorectal cancer (HNPCC/Lynch) syndrome. Despite the name, patients with HNPCC have polyps but many fewer than those patients with APC syndrome.

Imaging Studies

• Air contrast barium enema.
• • This test can detect larger polyps but can miss smaller ones; it has a low false-positive rate.
  • In a recent study, air contrast barium enema detected only about 50% of polyps greater than 1 cm in diameter.
• Virtual colonoscopy
• • This test is performed by CT scanning or MRI and has shown promise in research studies, detecting more than 80% of large polyps. In a recent large, multicenter trial, however, a disappointing sensitivity of only 55% was obtained for polyps 10 mm or larger in diameter.
  • In most methods, a thorough colon preparation is required, and colonoscopy must be subsequently performed to remove the lesions. Methods are under development to label stool with barium meals, obviating the need for cathartic bowel prep.

Procedures

• Adequate bowel cleansing is necessary prior to many procedures. Several preparations are marketed for bowel cleansing (eg, polyethylene glycol 3350 [GoLYTELY, NuLYTELY], magnesium citrate [Citroma], senna [X-Prep]) in preparing patients for surgery or gastrointestinal procedures such as endoscopy, colonoscopy, and barium x-ray studies. Bowel cleansing preparations may be used with various dietary preparations (eg, clear liquid diet 1-2 d before surgery or procedure) and are convenient to administer on an outpatient basis.
• Flexible sigmoidoscopy
• • Flexible sigmoidoscopy is a good screening test and the only procedure or imaging modality to be validated by studies that document a decrease in colorectal cancer mortality. However, this procedure does not examine the entire colon. Recent studies indicate that the majority of large adenomatous polyps in women will be missed by using flexible sigmoidoscopy alone.
  • Screening is usually begun at age 50 years in patients who are at average risk.
  • Randomized controlled trials have documented a reduction in mortality from colon cancer in populations screened by flexible sigmoidoscopy. However, recent studies suggest that about 40% of high-risk proximal adenomas remain undetected when this procedure is used as the primary screening modality.
• Colonoscopy
• • This is the preferred test to detect colonic polyps, obtain biopsies, and/or perform endoscopic resection. Sensitivities for large polyps in the 80-90% range have been reported.
  • Although flexible sigmoidoscopy and stool tests for occult blood have been the mainstays of screening to prevent colon cancer, some clinicians now favor colonoscopy as a primary screening tool.

Histologic Findings

Adenomatous polyps are of 3 different histological types: tubular, villous, and tubulovillous. Adenomatous polyps may show changes of dysplasia, which distinguish them from hyperplastic polyps. The most common benign polyp is hyperplastic.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Some studies have demonstrated that medical treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) decreases the number and size of polyps. However, NSAIDs, such as sulindac, do not prevent cancer development. These drugs do not yet constitute established therapies or chemopreventives for polyps.

Surgical Care

• Polypectomy
  • In the case of a solitary pedunculated polyp, colonoscopic removal can be performed concurrently with the search for other lesions.
  • Removal of a solitary polyp is usually curative for that lesion. However, a complete colonoscopic examination should be performed because the finding of a single adenomatous polyp confers an increased risk for the development of others. The rate of polyp recurrence (discovered at follow-up colonoscopy) at 1-year postpolypectomy is small, and recurrence may in fact represent missed synchronous lesions.
  • Most gastroenterologists now advocate repeat colonoscopy 5 years following complete removal of a low-risk adenomatous polyp (as defined histologically). Colonoscopy is repeated in 3 years if the polyp has high-risk features. If no polyps are found at the initial examination, follow-up colonoscopy at approximately 5-year intervals is recommended.
• Colonic resection
• • In the case of multiple intestinal polyps associated with FAP, resection remains the only feasible option.
  • Colonic resection is also advocated for patients with long-standing ulcerative colitis who have developed high-grade dysplasia or a dysplasia-associated lesion or mass (DALM).
  • Discuss several surgical options with the patient, including total colectomy versus subtotal colectomy with rectal sparing.

Consultations

• Surgical consultation
• • Consultation with a surgeon is critical in patients with multiple polyps, including patients with FAP.
  • Explain and discuss the type and timing of surgery with the patient.

Diet

A regular diet may be continued. The patient can consider calcium and folate supplements to decrease the risk of polyp recurrence.

Activity

Activities may be maintained as tolerated.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 polyp regression and to determine why they do not appear to prevent cancer development.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Provide further inpatient care as needed.

Further Outpatient Care

• Screening for recurrence is recommended through follow-up care with a gastroenterologist.
• See Villous Adenoma for more follow-up recommendations.

Deterrence/Prevention

• Currently, no firm guidelines exist regarding the prevention of the development of colonic polyps. Calcium and folate may be modestly protective. Fiber may also have some activity; the best evidence is for cereal fiber.
• Recent studies have demonstrated that a diet high in antioxidants has no impact on polyp recurrence.

Prognosis

• Colonic polyps are curable if removed. If not treated, the patient may develop complications such as bleeding, and the condition may even be fatal if malignant transformation occurs.
• Fortunately, polyps grow slowly; cancer development is estimated to usually occur about 10 years after formation of a small polyp.
• HNPCC is an exception. Progression to cancer appears to be more rapid because of increased genetic instability in the lesion. Patients with a HNPCC should undergo screening for polyps at more frequent intervals (every 1-2 y) than patients at average risk.

Patient Education

• Patients with a family history of colonic polyps must be aware of the potential benefits of screening for polyps.
• Patients with FAP must be aware of the potential benefits of screening the upper GI tract and screening family members, beginning at puberty, for the mutant APC gene. Screening is particularly important because of the inevitable development of colon cancer in affected individuals and the benefits associated with colonic resection.
• Patients with HNPCC are at risk for development of tumors at additional sites, including the uterus and ovaries. These patients should consider screening for tumor development at such sites or prophylactic resection.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• The ability to prevent colon cancer by polypectomy implies a responsibility to do so when possible. No screening tool is 100% effective; inevitably, polyps will be missed. However, once detected, ensuring that the lesion does not develop into a cancer is generally within the physician's ability.
• The efficacy of removal of pedunculated polyps by polypectomy can usually be accurately assessed by histology. In contrast, sessile lesions are often removed in pieces or have cautery artifact precluding correct determination of the resection margin. If the endoscopist is uncertain whether a lesion has been eliminated, follow-up colonoscopy in about 6 months to 1 year may be advisable (a shorter period if malignancy is suspected). Otherwise, a repeat colonoscopy in 3 years is usually advised.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Beach R, Chan AO, Wu TT, et al. BRAF mutations in aberrant crypt foci and hyperplastic polyposis. Am J Pathol. Apr 2005;166(4):1069-75.
• Bussey HJ, DeCosse JJ, Deschner EE. A randomized trial of ascorbic acid in polyposis coli. Cancer. Oct 1 1982;50(7):1434-9. [Medline].
• Cohen LB. A color atlas of colorectal lesions. In: Pazdur R, Hoskins WJ, Wagman L, Coia LR, eds. Cancer Management: A multidisciplinary approach. Huntington, NY:. Publisher Research & Representation, Inc;2000:301-305.
• Coia LR, Ellenhorn JDI, Ayoub JP. Colorectal and anal cancers. In: Pazdur R, Hoskins WJ, Wagman L, Coia LR, eds. Cancer Management: A multidisciplinary approach. Huntington, NY:. Publisher Research & Representation, Inc;2000:273-299.
• Cotran RS, Kumar V, Robbins SL. Tumors of the Small and Large Intestines. In: Cotran R, Kumar V, Robbins S, eds. Pathologic Basis of Disease. 5th ed. Philadelphia, Pa:. WB Saunders Company;1994:809-822.
• Giardiello FM, Offerhaus GJ, DuBois RN. The role of nonsteroidal anti-inflammatory drugs in colorectal cancer prevention. Eur J Cancer. Jul-Aug 1995;31A(7-8):1071-6. [Medline].
• Itzkowitz SH, Kim YS. Colonic Polyps and Polyposis Syndromes. In: Feldman M, Sleisenger MH, Scharschmidt BF, eds. Sleisinger & Fordtran's Gastrointestinal and Liver Disease; pathophysiology, diagnosis, management. Vol 2. 6th ed. Philadelphia, Pa:. WB Saunders Company;1998:1865-1905.
• Kinzler KW, Vogelstein B. Lessons from hereditary colorectal cancer. Cell. Oct 18 1996;87(2):159-70. [Medline].
• Ladabaum U, Song K. Projected national impact of colorectal cancer screening on clinical and economic outcomes and health services demand. Gastroenterology. Oct 2005;129(4):1151-62.
• Regueiro CR. AGA Future Trends Committee report: Colorectal cancer: a qualitative review of emerging screening and diagnostic technologies. Gastroenterology. Sep 2005;129(3):1083-103.
• Rex DK, Kahi CJ, Levin B, et al. Guidelines for colonoscopy surveillance after cancer resection: a consensus update by the American Cancer Society and the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology. May 2006;130(6):1865-71.
• Stryker SJ, Wolff BG, Culp CE. Natural history of untreated colonic polyps. Gastroenterology. Nov 1987;93(5):1009-13. [Medline].
• Winawer SJ, Zauber AG, Fletcher RH, et al. Guidelines for colonoscopy surveillance after polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society. Gastroenterology. May 2006;130(6):1872-85.

Article Last Updated: Jul 6, 2006