- Top of page
- Epidemiology of H. pylori and reflux disease
- H. pylori infection and gastric acid secretion
- Effect of H. pylori eradication on 24-h oesophageal pH and motility
- H. pylori eradication and the development of reflux disease
- H. pylori and the treatment of reflux disease
- Effect of H. pylori eradication on relapse in patients with established gastro- oesophageal reflux disease
- H. pylori and gastric atrophy in reflux disease
- H. pylori and reflux complications: barrett's oesophagus and oesophageal adenocarcinoma
- Does the cagA status matter?
The falling prevalence of Helicobacter pylori infection and related diseases (peptic ulcer disease, gastric cancer) in developed countries has been paralleled by an increased recognition of gastro-oesophageal reflux and its complications. These epidemiological data do not support a role for H. pylori in the pathogenesis of reflux disease, but suggest a negative association with the increasing incidence of oesophageal diseases. This has led some investigators to propose a ‘protective’ role of H. pylori infection against the development of oesophageal diseases. In these patients, pre-existing lower oesophageal sphincter dysfunction, susceptibility to reflux, unmasking of latent reflux and the patterns and severity of gastritis are probably important factors contributing to the development of oesophageal diseases. The most likely mechanism by which H. pylori infection may protect against reflux is by decreasing the potency of the gastric refluxate in patients with corpus-predominant gastritis. The prevalence of H. pylori infection in patients with reflux disease is probably no greater than that in those without reflux, and there are conflicting data indicating that reflux symptoms or erosive oesophagitis develop after H. pylori eradication. It is also unclear whether H. pylori augments the antisecretory effects of proton pump inhibitors or accelerates the development of atrophic gastritis.