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Helicobacter Pylori Infection and the Risk of Barrett's Oesophagus: A Community-Based Study
  1. Douglas A Corley (douglas.corley{at}kp.org)
  1. Kaiser Permanente Division of Research, United States
    1. Ai Kubo (ai.kubo{at}kp.org)
    1. Columbia University, Mailman School of Public Health, United States
      1. Theodore R Levin (trl{at}dor.kaiser.org)
      1. Kaiser Permanente Division of Research, United States
        1. Gladys Block (gblock{at}berkeley.edu)
        1. University of California, Berkeley, United States
          1. Laurel Habel (lah{at}dor.kaiser.org)
          1. Kaiser Permanente Division of Research, United States
            1. Wei Zhao (wkz{at}dor.kaiser.org)
            1. Kaiser Permanente Division of Research, United States
              1. Pat Leighton (pxl{at}dor.kaiser.org)
              1. Kaiser Permanente Division of Research, United States
                1. Gregory Rumore (gregory.rumore{at}kp.org)
                1. Kaiser Permanente, Oakland Medical Center, United States
                  1. Charles Quesenberry (charles.quesenberry{at}kp.org)
                  1. Kaiser Permanente Division of Research, United States
                    1. Patricia Buffler (pab{at}berkeley.edu)
                    1. University of California, Berkeley, United States
                      1. Julie Parsonnet (parsonnt{at}stanford.edu)
                      1. Stanford University, United States

                        Abstract

                        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.

                        • Barrett's
                        • adenocarcinoma
                        • esophageal or oesophageal
                        • helicobacter
                        • reflux

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