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pubmed-article:9707051pubmed:abstractTextThere is strong evidence accumulating that chronic infection with Helicobacter pylori (H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis.lld:pubmed
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pubmed-article:9707051pubmed:articleTitleEffects of Helicobacter pylori on gastritis, pentagastrin-stimulated gastric acid secretion, and meal-stimulated plasma gastrin release in the absence of peptic ulcer disease.lld:pubmed
pubmed-article:9707051pubmed:affiliationGastrointestinal Unit, Inselspital, Berne, Switzerland.lld:pubmed
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