SUCRALFATE SUPPRESSES HELICOBACTER-PYLORI INFECTION AND REDUCES GASTRIC-ACID SECRETION BY 50-PERCENT IN PATIENTS WITH DUODENAL-ULCER

Background & Aims: The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear. The aim of this study was to determine the ef fect of sucralfate on Helicobacter pylori infection and on the accompa nying hypersecretion of gastric acid the infection induces in patients with duodenal ulcer. Methods: Basal and gastrin-releasing peptide (GR P) stimulated gastrin release and acid secretion. H. pylori density, g astric urease activity, and severity of gastritis were studied in pati ents with duodenal ulcer who were positive for H. pylori before, durin g, and after 4 weeks' treatment with sucralfate (2 g twice daily). Res ults: The density of H. pylori decreased by 70% during sucralfate trea tment and returned to the pretreatment level after discontinuation of therapy. This suppression of H. pylori infection was accompanied by an 80% decrease in gastric urease activity. GRP-stimulated plasma gastri n concentrations, GRP-stimulated acid output, and basal acid output al l decreased by approximately 50% during sucralfate therapy and returne d to pretreatment levels after treatment was discontinued. Conclusions : These findings indicate that sucralfate markedly suppresses H. pylor i infection and the accompanying hypersecretion of acid the infection induces in patients with duodenal ulcer. These effects are likely to b e important mechanisms by which the drug promotes duodenal ulcer heali ng.