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Helicobacter pylori Infection and the Risk for Duodenal and Gastric Ulceration

Abraham Nomura, MD; Grant N. Stemmermann, MD; Po-Huang Chyou, PhD; Guillermo I. Perez-Perez, DSc; and Martin J. Blaser, MD
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From Kuakini Medical Center, Honolulu, Hawaii; the University of Cincinnati School of Medicine, Cincinnati, Ohio; the Vanderbilt University School of Medicine, Nashville, Tennessee. Requests for Reprints: Abraham Nomura, MD, the Japan-Hawaii Cancer Study, Kuakini Medical Center, 347 North Kuakini Street, Honolulu, HI 96817. Acknowledgments: The authors thank the Honolulu Heart Program for the use of its data and the following institutions for their cooperation: Castle Medical Center, Kaiser Medical Center, Pali Momi Medical Center, Queen's Medical Center, St. Francis Hospital, Straub Clinic and Hospital, Tripler Medical Center, and Wahiawa General Hospital. Grant Support: In part by grant R01 CA 33644 from the National Cancer Institute, National Institutes of Health; by the Medical Research Service of the Department of Veterans Affairs; and by the Proctor & Gamble Company.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;120(12):977-981. doi:10.7326/0003-4819-120-12-199406150-00001
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Objective: To determine whether a preexisting Helicobacter pylori infection increases the risk for developing duodenal or gastric ulcer.

Design: A nested case–control study based on a cohort of 5443 Japanese-American men who had a physical examination and a phlebotomy from 1967 to 1970.

Setting: All 10 general hospitals on the Hawaiian island of Oahu.

Patients: 150 patients with gastric ulcer and 65 patients with duodenal ulcer identified in the cohort of study participants after a hospital surveillance period of more than 20 years.

Measurements: Stored serum specimens from patients and from matched controls were tested for the presence of serum IgG antibody to H. pylori using enzyme-linked immunosorbent assay.

Results: 93% of the 150 patients with gastric ulcer and 78% of the matched controls had a positive antibody level for H. pylori–specific IgG, yielding an odds ratio of 3.2 (95% CI, 1.6 to 6.5). For duodenal ulcer, 92% of the 65 patients and 78% of the matched controls had a positive test result, yielding an odds ratio of 4.0 (CI, 1.1 to 14.2). As the level of antibody to H. pylori increased, a statistically significant increase was noted in the risk for gastric and duodenal ulcer. The association with H. pylori infection was statistically significant for both types of ulcer, even when the diagnosis was made 10 or more years after the serum sample had been obtained.

Conclusion: Preexisting H. pylori infection increases the risk for subsequent development of either duodenal or gastric ulcer disease.





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