Archief Roodbont

Aspirin use is associated with an increase in complicated gastroduodenal ulcers from both topical and systemic effects. Topical effects include erosions and ulcerations that occur shortly after ingestion of aspirin. To test a novel approach to reducing topical aspirin-induced gastroduodenal damage, investigators conducted an industry-supported, multicenter, randomized, phase II trial of a drug-delivery system that covalently links aspirin to the lipophilic molecule phosphatidylcholine (PC), thus facilitating transit of the resultant aspirin-PC compound across the gastrointestinal (GI) mucosal layer.

A total of 204 healthy individuals (age range, 50–75) with age-related increased risk for nonsteroidal anti-inflammatory drug (NSAID)-induced gastroduodenal damage were included in the study. All participants underwent baseline endoscopy, received low-dose (325 mg/day) aspirin or aspirin-PC for 7 days, and then underwent a second endoscopy.

Fewer participants in the aspirin-PC group than in the aspirin group developed an ulcer (5.1% vs. 17.6%; P=0.0069) or developed either an ulcer or 6 erosions (the primary endpoint; 22.2% vs. 42.2%; P=0.0027). The authors concluded that using phospholipids to circumvent local mechanisms of mucosal damage from aspirin might provide an additional way to reduce the incidence of ulceration in high-risk individuals.

Comment: The immediate gastric mucosal local effects of aspirin (or other NSAIDs that are weak acids) have been well established. However, these effects have not been correlated with long-term risks for systemic prostaglandin inhibition. Whether reductions in immediate local damage from aspirin result in better long-term outcomes for patients at high risk for GI events remains to be determined.

— David J. Bjorkman, MD, MSPH (HSA), SM (Epid.)

Published in Journal Watch Gastroenterology December 10, 2010