title: Helicobacter pylori infection and gastroesophageal reflux in a population-based study (The HUNT Study).
abstract: OBJECTIVE
  It has been suggested that Helicobacter pylori infection may prevent gastroesophageal reflux, possibly through gastric atrophy. Since, however, previous results are contradictory and no population-based studies are available, the relationship between H. pylori and reflux remains uncertain. The aim of this study was to investigate this relationship in a population-based, nested, case-control study.
  
  
  METHODS
  From a cohort of 65,363 individuals, representing 71.2% of the adult population in the Norwegian county of Nord-Trondelag, we randomly selected 472 persons with recurrent reflux symptoms (cases) and 472 without such symptoms (controls). Occurrence of H. pylori and its virulence factor cagA was determined serologically, using an immunoblot assay. Gastric atrophy was assessed through serum levels of pepsinogen I. Odds ratios (OR) with 95% confidence intervals (CI), adjusted for potential confounding factors, represented relative risks.
  
  
  RESULTS
  H. pylori infection was not associated with a decreased risk of reflux symptoms (OR 1.1, 95% CI 0.8-1.6), irrespective of positive cagA status (OR 1.1, 95% CI 0.8-1.5). Gastric atrophy reduced the risk of reflux symptoms (OR 0.2, 95% CI 0.0-0.6). Infection with H. pylori entailed a ninefold increase in the risk of gastric atrophy compared to non-infection (OR 8.9, 95% CI 2.0-39.9).
  
  
  CONCLUSIONS
  H. pylori infection, irrespective of cagA status, did not affect the occurrence of reflux symptoms in this population-based setting. Infected individuals are at increased risk of gastric atrophy, which in turn reduces reflux symptoms, but due to the low frequency of gastric atrophy among infected individuals overall, there was no association with reflux symptoms on a population level.
authors.affiliation: Unit of Esophageal and Gastric Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. helena.nordenstedt@ki.se
authors.forename: Helena
authors.initials: H
authors.lastname: Nordenstedt
authors.forename: Magnus
authors.initials: M
authors.lastname: Nilsson
authors.forename: Roar
authors.initials: R
authors.lastname: Johnsen
authors.forename: Jesper
authors.initials: J
authors.lastname: Lagergren
authors.forename: Kristian
authors.initials: K
authors.lastname: Hveem
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000276:immunology; D001284:Atrophy / Q000209:etiology / Q000473:pathology; D001426:Bacterial Proteins / Q000276:immunology; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000453:epidemiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications / Q000453:epidemiology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009664:Norway / Q000453:epidemiology; D020116:Pepsinogen A / Q000097:blood; D012307:Risk Factors; D016036:Seroepidemiologic Studies; D011795:Surveys and Questionnaires
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori; D020116:Pepsinogen A