HELICOBACTER-PYLORI INFECTION AND ABNORMALITIES OF ACID-SECRETION IN PATIENTS WITH DUODENAL-ULCER DISEASE

Background and Aims: The mechanism by which Helicobacter pylori predis poses to duodenal ulcers (DUs) remains unclear. The aim of this study was to investigate the effect of the infection on acid secretion. Meth ods: Acid output was examined basally and in response to gastrin-relea sing peptide (GRP) and gastrin in healthy volunteers with and without H. pylori infection and in patients with DUs before and after eradicat ion of the infection. Results: Compared with H. pylori-negative health y volunteers, patients with DUs with H. pylori had the following abnor malities of acid secretion: (1) threefold increase in basal acid outpu t, (2) sixfold increase in acid response to GRP, (3) increased maximal acid response to exogenous gastrin, (4) increased ratio of basal acid output to maximal gastrin-stimulated output, and (5) increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated ou tput. All of these abnormalities resolved fully after H. pylori eradic ation except for increased maximal acid output to gastrin, which was u nchanged. Infected healthy volunteers showed a threefold increase in a cid response to GRP that resolved after eradication of H. pylori infec tion. Conclusions: These disturbances in acid secretion caused by H. p ylori infection are consistent with impaired inhibitory control and ar e likely to be relevant to the mechanism by which the infection predis poses to DU.