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Rheumatology Advance Access originally published online on April 16, 2003
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Rheumatology 2003; 42: 947-950
© 2003 British Society for Rheumatology

Prevalence of Helicobacter pylori in NSAID users with gastric ulcer

Y. Matsukawa, M. Aoki, S. Nishinarita, S. Sawada, T. Horie, K. Kato1, Y. Kawamura1, F. Kawamura1, Y. Arakawa1, H. Kurosaka2, K. Morita3, E. Ohtsuka4, M. Oribe5, M. Nakano6 and Y. Kitami6

Department of Internal Medicine I,
1 Department of Internal Medicine III, Nihon University School of Medicine,
2 Kurosaka Clinic, Itabashi, Tokyo,
3 Morita Clinic, Kasukabe City, Saitama,
4 Ohtsuka Rheumatism Clinic,
5 Ohita Red Cross Hospital, Ohita City, Ohita and
6 Ohmiya Medical Association Hospital, Ohmiya, Saitama, Japan

Objective. Regarding the interaction of Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs), we cannot accept unanimous conclusions in inducing gastric ulcer. We therefore evaluated the role of Helicobacter pylori and NSAIDs in inducing gastric ulcer.

Methods. Dyspeptic patients receiving NSAIDs underwent endoscopic examination. Gastric ulcer formation and H. pylori status were investigated. Biopsy specimens from the antrum and lower body of the stomach were prepared for the rapid urease test and pathological evaluation. Anti-H. pylori antibody was measured by enzyme-linked immunosorbent assay.

Results. Two hundred and twenty-six patients receiving NSAIDs (220 chronic and six on-demand users) underwent gastrofibrescopic examination. There were 110 patients with gastric ulcer and 111 non-ulcer patients with gastritis. The remaining five patients had neither. NSAID users with gastric ulcer showed a low prevalence of H. pylori compared with those without them [55/110 (50.0%) vs 79/111 (71.2%), P < 0.01]. The same tendency was seen when patients receiving low-dose aspirin and those with rheumatoid arthritis were analysed separately [13/29 (44.8%) vs 50/62 (80.6%), P < 0.01, and 11/33 (33.3%) vs 16/26 (61.5%), P < 0.06 with Yates' correction, respectively].

Conclusion. Helicobacter pylori infection appeared to be a risk factor for developing gastritis, but we found no evidence that it increases gastric ulcer formation in NSAID users with dyspepsia.

KEY WORDS: Aspirin, Gastric ulcer, Gastritis, Helicobacter pylori, Non-steroidal anti-inflammatory drugs, Rheumatoid arthritis.

Correspondence to: Y. Matsukawa, Department of Internal Medicine I, Nihon University School of Medicine, Oyaguchi-Kamimachi, Itabashi 173-8610, Tokyo, Japan. E-mail: m-2000{at}mbk.sphere.ne.jp


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