Abstract
H. pylori infection, both in normal healthy subjects and patients with duodenal ulcer, results in modest elevations of serum gastrin concentrations in the fasting state and quite substantial elevations after a meal or gastrin releasing peptide (GRP) stimulation. Cure of the infection leads to normalization of gastrin homeostasis. Acid secretion in response to a submaximal infusion of GRP is three-fold higher in H. pylori-infected normal subjects and six-fold higher in DU patients than in non-infected controls. These changes also normalize after cure of the infection. H. pylori infection appears to lead to increased basal acid output in some patients with duodenal ulcer while effects on peak acid output to pentagastrin remain under debate. With the possible exception of peak acid output, the abnormalities of gastrin and acid secretion reported for patients with duodenal ulcer are largely a result of infection with H. pylori.
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