TITLE

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

AUTHOR(S)
Corley, D. A.; Kubo, A.; Levin, T. R.; Block, G.; Habel, L.; Zhao, W.; Leighton, P.; Rumore, G.; Quesenberry, C.; Buffler, P.; Parsonnet, J.
PUB. DATE
June 2008
SOURCE
Gut;Jun2008, Vol. 57 Issue 6, p727
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
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 (GOAD) 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 GOAD patients and 299 population controls. Patients with Barrett's oesophagus were substantially less likely to have antibodies for H pylori (OR = 0.42, 95% Cl 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% Cl 0.00 to 0.201 and those with CagA+ strains (OR = 0.08, 95% Cl 0.02 to 0.35). The associations were diminished after adjustment for GOAD 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.
ACCESSION #
32531193

 

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