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Helicobacter pylori infection and the risk of Barrett’s oesophagus: a community-based study
  1. D A Corley1,2,
  2. A Kubo1,3,
  3. T R Levin1,
  4. G Block4,
  5. L Habel1,
  6. W Zhao1,
  7. P Leighton1,
  8. G Rumore1,
  9. C Quesenberry1,
  10. P Buffler4,
  11. J Parsonnet5
  1. 1
    Division of Research, Kaiser Permanente, Oakland, California, USA
  2. 2
    Department of Medicine and Comprehensive Cancer Center, University of California, San Francisco, California, USA
  3. 3
    Mailman School of Public Health, Columbia University, NY, USA
  4. 4
    School of Public Health University of California, Berkeley, California, USA
  5. 5
    Department of Medicine and Department of Health Research and Policy, Stanford University, California, USA
  1. Dr D A Corley, Division of Research, Kaiser Permanente, 2000 Broadway, Oakland, CA 94612, USA; Douglas.Corley{at}


Objective: Gastric colonisation with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. Its associations with Barrett’s oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma, were evaluated

Methods: A case–control study was carried out in the Kaiser Permanente Northern California population, a large health services delivery organisation. Persons with a new Barrett’s oesophagus diagnosis (cases) were matched to subjects with gastro-oesophageal reflux disease (GORD) without Barrett’s oesophagus and to population controls. Subjects completed direct in-person interviews and antibody testing for H pylori and its CagA (cytotoxin-associated gene product A) protein.

Results: Serological data were available on 318 Barrett’s oesophagus cases, 312 GORD patients and 299 population controls. Patients with Barrett’s oesophagus were substantially less likely to have antibodies for H pylori (OR = 0.42, 95% CI 0.26 to 0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMIs <25, OR = 0.03, 95% CI 0.00 to 0.20) and those with CagA+ strains (OR = 0.08, 95% CI 0.02 to 0.35). The associations were diminished after adjustment for GORD symptoms. The H pylori status was not an independent risk factor for Barrett’s oesophagus compared with the GORD controls.

Conclusions: Helicobacter pylori infection and CagA+ status were inversely associated with a new diagnosis of Barrett’s oesophagus. The findings are consistent with the hypothesis that H pylori colonisation protects against Barrett’s oesophagus and that the association may be at least partially mediated through GORD.

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  • Funding:United States National Institutes of Health RO1 DK63616 and K08 DK02697. The study sponsor reviewed the protocol, but did not participate in the collection, analysis or interpretation of the data.

  • Competing interests: None.

  • Ethics approval: The study and analyses were approved by the institutional review board.

  • Patient consent: All subjects provided written informed consent.