Is the sensitivity to gastric acid inhibition Helicobacter pylori status-dependent?

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.

To survey and discuss the available information on the interaction between H. pylori status and the sensitivity to inhibition of gastric acid secretion.

Literature review.

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 H2-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.

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.