title: Review article: Helicobacter pylori and reflux disease.
abstract: 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.
authors.affiliation: Division of Gastroenterology, University of Kansas School of Medicine, Veterans Affairs Medical Center, Kansas City, MO 64128-2295, USA. psharma@kumc.edu
authors.forename: P
authors.initials: P
authors.lastname: Sharma
authors.forename: N
authors.initials: N
authors.lastname: Vakil
mesh_terms: D000230:Adenocarcinoma / Q000382:microbiology; D000942:Antigens, Bacterial; D001284:Atrophy / Q000382:microbiology; D001426:Bacterial Proteins; D001471:Barrett Esophagus / Q000382:microbiology; D004938:Esophageal Neoplasms / Q000382:microbiology; D005744:Gastric Acid / Q000378:metabolism; D005764:Gastroesophageal Reflux / Q000382:microbiology* / Q000503:physiopathology / Q000517:prevention & control; D005769:Gastrointestinal Motility / Q000502:physiology; D016481:Helicobacter Infections / Q000150:complications* / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D006863:Hydrogen-Ion Concentration; D012008:Recurrence; D013270:Stomach / Q000473:pathology
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori