{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,25]],"date-time":"2025-12-25T21:25:23Z","timestamp":1766697923401,"version":"3.48.0"},"reference-count":59,"publisher":"BMJ","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"accepted":{"date-parts":[[2000,12,5]]},"published-print":{"date-parts":[[2001,9,1]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND<\/jats:title>\n                    <jats:p>\n                      Helicobacter pylori is a gastroduodenal pathogen associated with ulceration, dyspepsia, and adenocarcinoma. Recent preliminary studies have suggested that\n                      <jats:italic>H pylori<\/jats:italic>\n                      may be protective for oesophageal adenocarcinoma. In addition, strains of\n                      <jats:italic>H pylori<\/jats:italic>\n                      identified by the presence of the cytotoxin associated gene A (\n                      <jats:italic>cagA<\/jats:italic>\n                      ) are shown to have a significant inverse association with oesophageal adenocarcinoma. Given that\n                      <jats:italic>cagA<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      <jats:italic>H pylori<\/jats:italic>\n                      may protect against oesophageal carcinoma, these strains may be protective for oesophagitis, a precursor of oesophageal carcinoma.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>AIMS<\/jats:title>\n                    <jats:p>\n                      The aim of this study was to investigate the association between\n                      <jats:italic>cagA<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      <jats:italic>H pylori<\/jats:italic>\n                      and endoscopically proved oesophagitis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>PATIENTS<\/jats:title>\n                    <jats:p>The study group included 1486 patients attending for routine upper gastrointestinal tract endoscopy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec sec-type=\"methods\">\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      At endoscopy the oesophagus was assessed for evidence of reflux disease and graded according to standard protocols. Culture and histology of gastric biopsy specimens determined\n                      <jats:italic>H pylori<\/jats:italic>\n                      status. The prevalence of\n                      <jats:italic>cagA<\/jats:italic>\n                      was identified by an antibody specific ELISA (Viva Diagnostika, Germany).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      H pylori was present in 663\/1485 (45%) patients and in 120\/312 (38%) patients with oesophagitis. Anti-CagA antibody was found in 499\/640 (78%)\n                      <jats:italic>H pylori<\/jats:italic>\n                      positive patients. Similarly, anti-CagA antibody was found in 422\/521 (81%) patients with a normal oesophagus and in 42\/60 (70%) with mild, 24\/35 (69%) with moderate, and 11\/24 (46%) with severe oesophagitis. The risk of severe oesophagitis was significantly decreased for patients infected with\n                      <jats:italic>cagA<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      <jats:italic>H pylori<\/jats:italic>\n                      after correction for confounding variables (odds ratio 0.57, 95% confidence interval 0.41\u20130.80; p=0.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>\n                      These results suggest that infection by\n                      <jats:italic>cagA<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      <jats:italic>H pylori<\/jats:italic>\n                      may be protective for oesophageal disease.\n                    <\/jats:p>\n                  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S","family":"Uff","sequence":"additional","affiliation":[{"name":"aPublic Health Laboratory, Gloucestershire Royal Hospital, Gloucester, UK, \n\nbGloucester Gastroenterology Group, Gloucestershire Royal Hospital, Gloucester, UK, \n\ncDepartment of Histopathology, Gloucestershire Royal Hospital, Gloucester, UK, \n\ndPHLS Statistics Unit, 61 Colindale Avenue, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N A","family":"Shepherd","sequence":"additional","affiliation":[{"name":"aPublic Health Laboratory, Gloucestershire Royal Hospital, Gloucester, UK, \n\nbGloucester Gastroenterology Group, Gloucestershire Royal Hospital, Gloucester, UK, \n\ncDepartment of Histopathology, Gloucestershire Royal Hospital, Gloucester, UK, \n\ndPHLS Statistics Unit, 61 Colindale Avenue, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H","family":"Barr","sequence":"additional","affiliation":[{"name":"aPublic Health Laboratory, Gloucestershire Royal 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