Helicobacter pylori infection and the risk of Barrett’s oesophagus: a community-based study

• Published in: Gut Vol. 57; no. 6; pp. 727 - 733
• Main Authors: Corley, D A, Kubo, A, Levin, T R, Block, G, Habel, L, Zhao, W, Leighton, P, Rumore, G, Quesenberry, C, Buffler, P, Parsonnet, J
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.06.2008; BMJ; BMJ Publishing Group LTD
• Subjects: Adenocarcinoma - complications; Adult; Aged; Antibodies, Bacterial - blood; Antigens, Bacterial - immunology; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Bacterial Proteins - immunology; Barrett Esophagus - complications; Bias; Biological and medical sciences; Biopsy; Carcinogens; Case-Control Studies; Endoscopy; Esophageal Neoplasms - complications; Esophagus; Family medical history; Female; Gastroenterology. Liver. Pancreas. Abdomen; Gastroesophageal Reflux - complications; Helicobacter Infections - complications; Helicobacter pylori; Helicobacter pylori - immunology; Human bacterial diseases; Humans; Infections; Infectious diseases; Male; Medical sciences; Middle Aged; Mucous membrane; Other diseases. Semiology; Pathology; Population; Precancerous Conditions - complications; Risk Assessment - methods; Studies; Ulcers; Northern California; Infection; Premalignant lesion; Spirillales; Helicobacter pylori; Esophageal disease; Risk factor; Gastroenterology; Barrett's esophagus; Spirillaceae; Bacteria; Digestive diseases
• ISSN: 0017-5749; 1468-3288
• DOI: 10.1136/gut.2007.132068

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 <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.