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Prevention of Aspirin-Related Gastric Ulcers

 Mar 22, 2012 Viewed: 489

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.

Ulcer complications associated with anti-inflammatory drug use. What is the extent of the disease burden? Information on the intake of non-steroidal anti-inflammatory drugs (NSAIDs) and on aspirin taken regularly by patients with peptic ulcer bleeding aged 60 years and over was used in conjunction with data measuring the overall frequency of hospital admissions with ulcer bleeding in England and Wales to determine the annual burden of disease imposed by particular treatment strategies. Over 40% of the calculated 8528 episodes of ulcer bleeding in those aged 60 years and over, and over 40% of the estimated 981 deaths each year would seem to be causally related to the treatments. Substitution of the NSAID with the lowest associated risk would be expected to reduce the frequency of non-aspirin NSAID-associated episodes of ulcer bleeding, and deaths, each by over 70%. Use of the lowest conventional dose of regular prophylactic aspirin (75 mg) would also be expected to reduce the frequency of treatment-related episodes, and deaths, by nearly 30%. Both strategies employed together would be expected to reduce NSAID and regular aspirin-related bleeding ulcer admissions from 4121 to less than 2184, and deaths from 523 to less than 250. Substitution of completely safe anti-inflammatory analgesics and anti-platelet drugs would be expected to reduce admissions from 4121 to 1072, and deaths from 523 to 123. ### Langman MJ.
### References Ng F-H et al: Famotidine is inferior to pantoprazole in preventing recurrence of aspirin-related peptic ulcers or erosions. Gastroenterology 138:82, 2010 ### Kurt J. Isselbacher Distinguished Mallinckrodt Professor of Medicine, Harvard Medical School; Physician and Director, Massachusetts General Hospital Cancer Center, Boston

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