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Contempo 1998
September 9, 1998

Antisecretory Therapy for Bleeding Peptic Ulcer

Author Affiliations

Author Affiliations: From the Department of Medicine, University of Texas Southwestern Medical School at Dallas and Medical Service, Department of Veterans Affairs Medical Center, Dallas (Dr Peterson), and Departments of Medicine and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario (Dr Cook). Dr Cook is a Consulting Editor, JAMA. Dr Peterson is an ad hoc consultant to and has received honoraria and research funds from Astra Merck and Glaxo Wellcome. Dr Cook has received research supplies from Glaxo Wellcome.


Edited by Ronna Henry Siegel, MD, Contributing Editor.

JAMA. 1998;280(10):877-878. doi:10.1001/jama.280.10.877

RECURRENT bleeding in patients hospitalized for bleeding peptic ulcer increases the need for surgery and the risk of death. The success of histamine2 (H2)–receptor antagonists in the treatment of symptomatic but uncomplicated peptic ulcer led to their widespread use in patients hospitalized for bleeding ulcers in the hope of preventing recurrent bleeding. In 1985, a landmark meta-analysis summarized the results of 27 randomized trials of cimetidine or ranitidine in 1673 patients with bleeding gastric or duodenal ulcer. The authors concluded that "treatment with H2-receptor antagonists appears to be moderately promising" and called for large-scale studies to confirm their benefit.1 Such a study was performed comparing intravenous famotidine with placebo in 1005 hospitalized patients whose ulcers showed signs of recent hemorrhage (SRH).2 Rebleeding rates were similar in each group, occurring in 24% of patients treated with famotidine and 26% of those treated with placebo. These results suggested either that the role of gastric acidity in in-hospital recurrent ulcer bleeding was inconsequential or that the reduction of gastric acidity afforded by H2-receptor antagonists was insufficient to prevent rebleeding. Support for the latter hypothesis came from in vitro data indicating that the integrity of the clot that stops ulcer bleeding in the first place would be best maintained at gastric pH levels near neutrality,3 a physiologic condition not easily achieved with H2-receptor antagonists.