Helicobacter pylori

Helicobacter pylori infection and the risk of Barrett’s oesophagus: a community-based study

D A Corley^1,2, A Kubo^1,3, T R Levin¹, G Block⁴, L Habel¹, W Zhao¹, P Leighton¹, G Rumore¹, C Quesenberry¹, P Buffler⁴, J Parsonnet⁵

¹ Division of Research, Kaiser Permanente, Oakland, California, USA
² Department of Medicine and Comprehensive Cancer Center, University of California, San Francisco, California, USA
³ Mailman School of Public Health, Columbia University, NY, USA
⁴ School of Public Health University of California, Berkeley, California, USA
⁵ Department of Medicine and Department of Health Research and Policy, Stanford University, California, USA

Dr D A Corley, Division of Research, Kaiser Permanente, 2000 Broadway, Oakland, CA 94612, USA; Douglas.Corley{at}kp.org

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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