AGI December 40/6

Feldman, Mark, Byron Cryer, Doug Sammer, Edward Lee, and Stuart J. Spechler. Influence of H. pylori infection on meal-stimulated gastric acid secretion and gastroesophageal acid reflux. Am. J. Physiol. 277 (Gastrointest. Liver Physiol. 40): G1159–G1164, 1999.—Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylori gastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased ,20 mmol/l in subjects whose infection was eradicated (P , 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylori eradication, despite a 41% reduction in meal-stimulated gastrin release (P , 0.05). Gastroesophageal acid reflux increased twoto threefold after successful treatment (P , 0.05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux.