Intestinal Polypoid Adenomas Medication

Updated: Feb 05, 2018
  • Author: Swati G Patel, MD, MS; Chief Editor: BS Anand, MD  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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

Sulindac (Clinoril)

Sulindac is a sulfoxide that is metabolized to the anti-inflammatory sulfide metabolite and a sulfone metabolite. Both metabolites are known to have apoptotic activity on the colonic epithelial cells, but whether this is required for the chemoregressive activity of these drugs is not known. It has multiple systemic effects, including analgesia, antipyretic, and anti-inflammatory, mostly mediated by the inhibition of prostaglandin synthesis.

Celecoxib (Celebrex)

Celecoxib inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. It has multiple systemic effects, including analgesia, antipyretic, and anti-inflammatory, mostly mediated by the selective inhibition of prostaglandin synthesis.

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