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High incidence of reflux oesophagitis after eradication therapy for Helicobacter pylori : impacts of hiatal hernia and corpus gastritis
Author(s) -
Hironobu Hamada,
Ken Haruma,
Mitsuhiro Mihara,
Takenobu Kamada,
Masaharu Yoshihara,
Koji Sumii,
Goro Kajiyama,
Masahiro Kawanishi
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.00758.x
Subject(s) - medicine , hiatal hernia , helicobacter pylori , gastroenterology , gastritis , esophagitis , atrophic gastritis , reflux esophagitis , reflux , hernia , endoscopy , surgery , disease
Background: Although several recent studies have shown that the eradication of Helicobacter pylori provokes reflux oesophagitis, the results are conflicting. Aim: To investigate the prevalence of reflux oesophagitis in patients after eradication of H. pylori and consider its association with hiatal hernia and corpus gastritis. Methods: A total of 286 patients who underwent H. pylori eradication therapy and 286 age‐ and disease‐matched H. pylori ‐positive controls who did not undergo eradication therapy were followed prospectively. All patients and controls underwent endoscopy at 1‐year intervals or when upper gastrointestinal symptoms recurred. The presence of hiatal hernia and histology of the gastric corpus were evaluated at the time of initial endoscopy. Results: The estimated prevalence of reflux oesophagitis within 3 years was 18% after eradication therapy and 0.3% without therapy. Patients who developed reflux oesophagitis after therapy had a greater prevalence of hiatal hernia ( P =0.0008) and more severe corpus gastritis ( P =0.0005) before therapy. Cumulative prevalence of reflux oesophagitis was 26% in patients with hiatal hernia, 7.7% in those without hiatal hernia, 33% in those with corpus atrophic gastritis and 13% in those without corpus atrophic gastritis. When patients had both hiatal hernia and corpus gastritis, the prevalence of reflux oesophagitis was 37%. The newly developed reflux oesophagitis was classified as mild in 35 out of 36 (97%) patients who developed reflux oesophagitis after eradication therapy. Conclusions: Eradication of H. pylori increased the prevalence of reflux oesophagitis in our patient group. The presence of hiatal hernia and corpus gastritis are closely related to the development of reflux oesophagitis after H. pylori eradication therapy.