{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T17:18:02Z","timestamp":1779211082503,"version":"3.51.4"},"reference-count":70,"publisher":"BMJ","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>\n                      Gastric colonisation with the\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      bacterium is a proposed protective factor against oesophageal adenocarcinoma, but its point of action is unknown. Its associations with Barrett\u2019s oesophagus, a metaplastic change that is a probable early event in the carcinogenesis of oesophageal adenocarcinoma, were evaluated\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      A case\u2013control study was carried out in the Kaiser Permanente Northern California population, a large health services delivery organisation. Persons with a new Barrett\u2019s oesophagus diagnosis (cases) were matched to subjects with gastro-oesophageal reflux disease (GORD) without Barrett\u2019s oesophagus and to population controls. Subjects completed direct in-person interviews and antibody testing for\n                      <jats:italic>H pylori<\/jats:italic>\n                      and its CagA (cytotoxin-associated gene product A) protein.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Serological data were available on 318 Barrett\u2019s oesophagus cases, 312 GORD patients and 299 population controls. Patients with Barrett\u2019s oesophagus were substantially less likely to have antibodies for\n                      <jats:italic>H pylori<\/jats:italic>\n                      (OR\u200a=\u200a0.42, 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\u200a=\u200a0.03, 95% CI 0.00 to 0.20) and those with CagA+ strains (OR\u200a=\u200a0.08, 95% CI 0.02 to 0.35). The associations were diminished after adjustment for GORD symptoms. The\n                      <jats:italic>H pylori<\/jats:italic>\n                      status was not an independent risk factor for Barrett\u2019s oesophagus compared with the GORD controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      infection and CagA+ status were inversely associated with a new diagnosis of Barrett\u2019s oesophagus. The findings are consistent with the hypothesis that\n                      <jats:italic>H pylori<\/jats:italic>\n                      colonisation protects against Barrett\u2019s oesophagus and that the association may be at least partially mediated through GORD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gut.2007.132068","type":"journal-article","created":{"date-parts":[[2007,10,12]],"date-time":"2007-10-12T14:13:02Z","timestamp":1192198382000},"page":"727-733","source":"Crossref","is-referenced-by-count":89,"title":["<i>Helicobacter pylori<\/i>\n                    infection and the risk of Barrett\u2019s oesophagus: a community-based study"],"prefix":"10.1136","volume":"57","author":[{"given":"D A","family":"Corley","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Kubo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T 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