Intestinal Polyposis Syndromes Medication

Updated: Apr 26, 2017
  • Author: Amit A Shah, MD; Chief Editor: Carmen Cuffari, MD  more...
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Medication

Medication Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, have been consistently associated with diminished risk of colorectal cancer. Sulindac has been reported to cause regression of adenomas in patients with Gardner syndrome. NSAIDs suppress cyclooxygenase-2 (COX-2), which affects epithelial proliferation and apoptosis.

Studies by Watanabe et al suggest an important role of antagonistic agents for the prostaglandin EP1 receptor for chemoprotection against the development of colon cancer. [47]

Many future therapies will target the actual signaling pathways disrupted by the affected genes in polyposis syndromes. For example, a trial studying rapamycin use in Cowden syndrome has been conducted. [27]

In additional to nutritional support, steroids have also been shown to be the mainstay of medical treatment that can lead to remission in Cronkhite-Canada syndrome. Azathioprine is also used as a steroid-sparing agent. [56]

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Nonsteroidal anti-inflammatory drugs (NSAIDs)

Class Summary

Growing evidence suggests a protective role for NSAIDs against the development of colorectal cancer. In addition, a significant effect in reversing adenoma growth has been illustrated with the use of sulindac and celecoxib in patients with FAP. Aspirin may also be useful to reduce the recurrence of polyps or cancer, but because of the potential for these drugs to cause damage to the upper gastrointestinal tract, they are not routinely recommended for this purpose.

Studies have shown that APC inactivation and EGFR signaling increase COX2 expression, which may lead to intestinal neoplasia. The mechanism of NSAID-induced polyp regression is not completely known, but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in prostaglandin synthesis although a non-COX mechanism may also contribute.

The mechanism of NSAID-induced polyp regression is not known, but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in prostaglandin synthesis although non-COX mechanism may also contribute.

Sulindac (Clinoril)

Has been reported to cause regression of adenomas in patients with Gardner syndrome (ie, FAP).

A recent study randomized patents to Sulindac 150 mg twice daily along with Erlotinib 75 mg daily versus placebo for 6 months and measured polyp burden. The patients on medications had a lower duodenal polyp burden at 6 months but many patients developed adverse events such as an acne-like rash, and it is unknown whether the medications prevent new duodenal adenomas from forming.

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Cyclooxygenase-2 (COX-2) inhibitors

Class Summary

These agents inhibit COX-2, thus suppress production of prostaglandin E2 at inflammation sites.

Celecoxib (Celebrex)

Recently was approved by the FDA for treatment of Gardner syndrome as an adjunct to endoscopy and surgery. The mean reduction in the number of polyps was 28% with 400 mg PO bid and 12% with 100 mg PO bid (5% placebo).

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