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. 2008 Jun;57(6):727-33.
doi: 10.1136/gut.2007.132068. Epub 2007 Sep 25.

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

D A Corley  1 , A Kubo, T R Levin, G Block, L Habel, W Zhao, P Leighton, G Rumore, C Quesenberry, P Buffler, J Parsonnet
Affiliations

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

D A Corley et al. Gut. 2008 Jun.

Abstract

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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Conflict of interest statement

Statement of competing interests: none to declare

References

    1. Blot WJ, McLaughlin JK. The changing epidemiology of esophageal cancer. Semin Oncol. 1999;26(5 Suppl 15):2–8. - PubMed
    1. Bollschweiler E, Wolfgarten E, Gutschow C, et al. Demographic variations in the rising incidence of esophageal adenocarcinoma in white males. Cancer. 2001;92(3):549–55. - PubMed
    1. Corley D, Buffler P. Oesophageal and gastric cardia adenocarcinomas: analysis of regional variation using the Cancer Incidence in Five Continents database. International Journal of Epidemiology. 2001;30:1415–25. - PubMed
    1. Kubo A, Corley DA. Marked regional variation in adenocarcinomas of the esophagus and the gastric cardia in the United States. Cancer. 2002;95(10):2096–102. - PubMed
    1. Sharma P, McQuaid K, Dent J, et al. A critical review of the diagnosis and management of Barrett’s esophagus: the AGA Chicago Workshop. Gastroenterology. 2004;127(1):310–30. - PubMed

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