Eradication ofHelicobacter pyloriInfection in Patients with Non-Ulcer Dyspepsia: Effects on Basal and Bombesin-Stimulated Serum Gastrin and Gastric Acid Secretion

Publisher Website
Google Scholar
Abstract
This study evaluates the effect of eradicating Helicobacter pylori on basal and bombesin-stimulated gastric acid secretion and serum gastrin in non-ulcer dyspepsia. Before and 1 month after an attempt to eradicate H. pylori basal and bombesin-stimulated gastric acid outputs were measured in 23 patients. H. pylori was eradicated in 15 patients (group A) but not in the other 8 (group B). Incremental gastric acid output was calculated by subtracting basal from bombesin-stimulated values. Basal acid output increased significantly (p = 0.01) after therapy in group A (delta 1.6 +/- 0.6 mmol/h) but not in group B (delta 0.2 +/- 0.5 mmol/h). Incremental gastric acid output decreased distinctly (delta-3.9 +/- 1.4 mmol/h) after therapy in group A (p = 0.02) but not in group B (delta-2.2 +/- 1.7 mmol/h). Basal serum gastrin decreased significantly (p < 0.005) after therapy in group A (delta-9 +/- 4 pM) but not in group B (delta-1 +/- 2 pM). Integrated serum gastrin responses to bombesin decreased markedly (p < 0.001) after therapy in group A (delta-5.0 +/- 1.6 nM*60 min) but slightly in group B (delta-0.9 +/- 1.3 nM*60 min) (p < 0.05). In patients with non-ulcer dyspepsia basal serum gastrin concentrations decrease but basal gastric acid outputs increase after eradication of H. pylori. Bombesin-induced increments in gastric acid output, however, decrease in parallel with gastrin release.