title: Helicobacter pylori: a debated factor in gastroesophageal reflux disease.
abstract: The prevalence of Helicobacter pylori infection is steadily decreasing in developing countries, and this has been paralleled by an increasing incidence of gastroesophageal reflux disease (GERD) and adenocarcinomas of the esophagus and of the esophagogastric junction. The prevalence of H. pylori infection, which is on the decline in Europe and in the United States, is probably related to improvements in sanitary conditions and socioeconomic status. These epidemiological data do not support a role for H. pylori in the pathogenesis of GERD, but at the same time suggest a negative association with the rising incidence in esophageal diseases. While H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from the development of GERD and its complications. There are conflicting reports that GERD can develop after H. pylori eradication and that proton pump inhibitors are less effective in suppressing intragastric acidity in H. pylori negative patients--reasons not to eradicate H. pylori in GERD patients. On the contrary, other data suggest an increase in the development of atrophic gastritis in GERD patients (H. pylori positive) on long-term proton pump inhibitor therapy - a reason to eradicate H. pylori. Preexisting lower esophageal sphincter dysfunction, susceptibility to GERD, unmasking of latent GERD, and patterns and severity of gastritis may be important factors contributing to the development of GERD rather than just the presence or absence of infection with H. pylori.
authors.affiliation: University of Kansas School of Medicine, Department of Veterans Affairs Medical Center, Kansas City, MO 64128, USA. psharma@kumc.edu
authors.forename: P
authors.initials: P
authors.lastname: Sharma
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology / Q000473:pathology; D000897:Anti-Ulcer Agents / Q000494:pharmacology; D001471:Barrett Esophagus / Q000209:etiology / Q000473:pathology; D005744:Gastric Acid / Q000378:metabolism; D005764:Gastroesophageal Reflux / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D011379:Prognosis; D054328:Proton Pump Inhibitors; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000209:etiology / Q000473:pathology
chemical_list: D000897:Anti-Ulcer Agents; D054328:Proton Pump Inhibitors