Prevention of Aspirin-Related Gastric Ulcers

Kurt J. Isselbacher

Disclosures

AccessMedicine from McGraw-Hill 

The use of low-dose aspirin in the prevention of cardiovascular disease is frequently associated with a development of dyspeptic symptoms and erosions or ulcerations in the upper GI tract. Eradication of Helicobacter pylori and maintenance therapy with proton pump inhibitors (PPIs) are effective in the prevention of aspirin-induced GI lesions. The potential role of H2-receptor antagonists after the healing of aspirin-induced ulcers or erosions is unclear.

Ng and colleagues (2010) have reported the results of a randomized, double-blind, controlled study comparing the efficacy of high-dose famotidine with that of pantoprazole in the prevention of recurrent dyspeptic/complicated ulcer or erosions in patients taking low-dose aspirin. Consecutive patients at a center in Hong Kong with a history of aspirin-related peptic disease with or without a history of bleeding were randomized to receive 80 mg of aspirin, with either 40 mg of famotidine or 20 mg of pantoprazole daily for 48 weeks. The endpoints were the presence of ulcer complications and the severity of ulcer complications. Those patients with peptic ulcerations received a healing dose of PPI for 8 weeks while those who were H. pylori positive received an initial 7-day standard PPI-based triple therapy followed by 7 weeks of PPI therapy alone.

Of a total of 161 patients who were randomized, 65 in each arm completed the study. The prevalence of significant dyspepsia or peptic ulceration was significantly higher in the famotidine group compared with the pantoprazole group (20% vs. 0%; p < .0001).

These findings demonstrate that high-dose famotidine therapy is inferior to PPI therapy in preventing recurrence of aspirin-related peptic ulcers or erosions. Thus, PPIs rather than H2-receptor antagonists are recommended in the prevention of recurrent low-dose aspirin–induced upper GI injury.

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