Objective: Gastric colonization with the Helicobacter pylori bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. We evaluated its associations with Barrett's oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma.
Design: A case-control study
Setting: The Kaiser Permanente Northern California population, a large health services delivery organization
Patients: Persons with a new Barrett's oesophagus diagnosis (cases) were matched to subjects with gastrooesophageal reflux disease (GORD) without Barrett's oesophagus and to population controls.
Main Measures: Subjects completed direct in-person interviews and antibody testing for Helicobacter pylori and its cagA protein.
Results: Serologic 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 Helicobacter pylori (odds ratio [OR] = 0.42, 95% confidence interval [CI] 0.26-0.70) than population controls; this inverse association was stronger among those with lower body mass indexes (BMI<25 OR=0.03, 95% CI 0.00 – 0.20) and those with cagA+ strains (OR=0.08, 95% CI 0.02-0.35). The associations were diminished after adjustment for GORD symptoms. The H. pylori status was not an independent risk factor for Barrett's oesophagus compared to 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 Helicobacter pylori colonization protects against Barrett's oesophagus and that the association may be at least partially mediated through GORD.
- esophageal or oesophageal
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