TY - JOUR T1 - <em>Helicobacter pylori</em> infection and the risk of Barrett’s oesophagus: a community-based study JF - Gut JO - Gut SP - 727 LP - 733 DO - 10.1136/gut.2007.132068 VL - 57 IS - 6 AU - D A Corley AU - A Kubo AU - T R Levin AU - G Block AU - L Habel AU - W Zhao AU - P Leighton AU - G Rumore AU - C Quesenberry AU - P Buffler AU - J Parsonnet Y1 - 2008/06/01 UR - http://gut.bmj.com/content/57/6/727.abstract N2 - 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 &lt;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. ER -