Is the Sensitivity to Gastric Acid Inhibition Helicobacter pylori Status-Dependent?

Abstract

Background: Recent studies using 24-h intragastric pH monitoring suggest that treatment with a proton-pump inhibitor is less effective in Helicobacter pylori -negative than in H. pylori -positive subjects. Aim : To survey and discuss the available information on the interaction between H. pylori status and the sensitivity to inhibition of gastric acid secretion. Methods: Literature review. Results: Upon cure of the infection in H. pylori -positive subjects (healthy controls and duodenal ulcer patients), the effect of omeprazole on gastric pH decreases significantly. The findings indicate that H. pylori or H. pylori -related gastritis augments the sensitivity to proton-pump inhibitors. Preliminary information suggests that the sensitivity to H 2 -receptor antagonists might be less dependent on H. pylori status. The mechanisms through which H. pylori or the H. pylori -associated gastritis leads to increased sensitivity to acid inhibition have not been fully elucidated. It has been hypothesized that the gastritis associated with H. pylori infection plays a role, since the mucosal inflammatory infiltrate can release acid inhibitory cytokines. Another possible mechanism involves the production of acid neutralizing substances by H. pylori , in particular ammonia. Ammonia might also interfere with the activity of the H + /K + -ATPase pump. Finally, H. pylori has been shown to produce fatty acids that inhibit the proton pump. Conclusions: An interaction exists between H. pylori status and sensitivity to acid inhibition. This interaction has important clinical implications. In H. pylori -negative patients, current dosing with a proton-pump inhibitor may result in insufficient acid control for optimal treatment of gastro-oesophageal reflux disease (GORD). In future studies on treatment and the natural course of GORD, H. pylori status must be taken into account.