Villous Adenoma Medication

Updated: Oct 24, 2016
  • Author: Alnoor Ramji, MD, FRCPC; Chief Editor: Burt Cagir, MD, FACS  more...
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Medication

Medication Summary

The literature supports the use of NSAIDs in FAP syndrome, with regression of polyps already present. It has been demonstrated that COX-2 is up-regulated 2-50 times in most (85-90%) adenocarcinomas. The role for NSAIDs (including the newer COX-2 inhibitors) in nonfamilial adenomatous lesions is unclear. For sporadic polyps, NSAID use has not been proven to cause regression in already developed polyps, although evidence suggests a decreased incidence of polyps in persons already taking NSAIDs. Therefore, a potential role exists for NSAIDs as primary prophylaxis.

In patients who have had a history of colon cancer, patients undergoing therapy with aspirin at 325 mg daily have fewer polyps than those on placebo. In patients with a history of a colonic polyp, low-dose aspirin (81 mg) may have some benefit in decreased adenoma recurrence. [9]

Studies with celecoxib have shown some regression in polyps in those patients with FAP. However, the routine use of COX-2 inhibitors for this indication may not be reasonable, especially in consideration of the recent documentation on cardiovascular toxicity/contraindications.

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Nonsteroidal anti-inflammatory drugs

Class Summary

Mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions, also may exist.

Sulindac (Clinoril)

Sulfoxide NSAID that is metabolized to the anti-inflammatory sulfide metabolite and a sulfone metabolite. Sulfide metabolite is now known to have apoptotic activity on colonic epithelial cells and is presumed to be responsible for regression of adenomatous polyps. Primary route of excretion is via urine as both sulindac and its sulfone metabolite.

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