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Changes in Helicobacter pylori ‐induced gastritis in the antrum and corpus during long‐term acid‐suppressive treatment in Japan
Author(s) -
Uemura N.,
Okamoto S.,
Yamamoto S.,
Matsumura N.,
Yamaguchi S.,
Mashiba H.,
Sasaki N.,
Taniyama K.
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.1365-2036.2000.00834.x
Subject(s) - medicine , gastroenterology , helicobacter pylori , gastritis , omeprazole , intestinal metaplasia , antrum , famotidine , biopsy , gastric acid , stomach
Background: Several studies have shown that acid‐suppressive therapy aggravates corpus gastritis in patients with Helicobacter pylori infection, promoting the development of atrophic gastritis. Aim: To study the effects of long‐term use of antisecretory agents on the H. pylori ‐positive gastric mucosa in Japan, a country with a high incidence of gastric cancer. Methods: A total of 141 H. pylori ‐positive patients who had peptic ulcers or reflux oesophagitis were treated for 3 years with either omeprazole (20 mg/day) alone ( n =7) or with omeprazole for primary therapy (8 weeks), followed by famotidine (40 mg/day) for maintenance therapy ( n =134). Endoscopy was performed before, during, and after treatment. Biopsy specimens were taken from the greater curvature of the antrum and corpus and were examined histologically. Results: The long‐term use of famotidine after 8 weeks of treatment with omeprazole distinctly decreased H. pylori density and neutrophil infiltration in the antrum, but did not change H. pylori density in the corpus. The gastritis score increased in patients who had no, or only mild corpus gastritis before treatment ( n =74), and significantly decreased in those who had moderate or severe gastritis before treatment ( n =60). In four of the seven patients who received long‐term treatment with omeprazole alone, neutrophil infiltration and H. pylori density decreased not only in the antrum but also in the corpus. There was no increase in intestinal metaplasia or mucosal atrophy as assessed endoscopically during follow‐up. Conclusion: Changes in corpus gastritis in response to acid‐suppressive therapy depend on the severity of gastritis before treatment. Long‐term use of acid‐suppressive therapy apparently does not accelerate the development of atrophy or intestinal metaplasia in Japanese patients.