Improvement in Atrophic Gastritis and Intestinal Metaplasia in Patients in Whom Helicobacter pylori Was Eradicated

  1. Toshifumi Ohkusa, MD;
  2. Kazuhiko Fujiki, MD;
  3. Ichizen Takashimizu, MD;
  4. Jiro Kumagai, MD;
  5. Toru Tanizawa, MD;
  6. Yoshinobu Eishi, MD;
  7. Tetsuji Yokoyama, MD; and
  8. Mamoru Watanabe, MD
  1. From School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

    Abstract

    Background: Glandular atrophy and intestinal metaplasia are precancerous lesions; whether Helicobacter pylori eradication affects these lesions is controversial.

    Objective: To determine whether H. pylori eradication is associated with improvement in glandular atrophy and intestinal metaplasia after at least 1 year.

    Design: Single-blind, uncontrolled prospective trial.

    Setting: Academic gastroenterology clinic in Japan.

    Patients: 163 consecutive patients with dyspepsia and H. pylori infection.

    Intervention: One-week course of a proton-pump inhibitor and antibiotic therapy.

    Measurements: Endoscopic examination with antral and corporal biopsy was done before treatment and at 1 to 3 and 12 to 15 months after treatment. Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System.

    Results: In the 115 patients in whom H. pylori was eradicated, inflammation and mean neutrophil activity had decreased by 1 to 3 months, and both glandular atrophy in the corpus and intestinal metaplasia in the antrum had decreased by 12 to 15 months. Glandular atrophy in the corpus improved in 34 (89%) of 38 patients with atrophy before treatment, and intestinal metaplasia in the antrum improved in 28 (61%) of 46 patients who had metaplasia at baseline. In the 48 patients in whom eradication was unsuccessful, no significant histologic changes were observed.

    Conclusion: In the year after successful H. pylori eradication, precancerous lesions improved in most patients.

    Article and Author Information

    • Grant Support: In part by Takeda Chemical Industries, Ltd., Osaka, Japan.

    • Requests for Single Reprints: Toshifumi Ohkusa, MD, Department of Gastroenterology and Hepatology, School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan; e-mail, ohkusa.gast{at}tmd.ac.jp.

    • Current Author Addresses: Drs. Ohkusa, Fujiki, Takashimizu, and Watanabe: Department of Gastroenterology and Hepatology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

    • Drs. Kumagai, Tanizawa, and Eishi: Department of Pathology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

    • Dr. Yokoyama: Department of Epidemiology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

    • Author Contributions: Conception and design: T. Ohkusa.

    • Analysis and interpretation of the data: T. Ohkusa, J. Kumagai, T. Tanizawa, Y. Eishi, T. Yokoyama.

    • Drafting of the article: T. Ohkusa.

    • Critical revision of the article for important intellectual content: T. Ohkusa, M. Watanabe.

    • Final approval of the article: T. Ohkusa, M. Watanabe.

    • Provision of study materials or patients: T. Ohkusa, K. Fujiki, I. Takashimizu.

    • Statistical expertise: T. Yokoyama.

    • Obtaining of funding: T. Ohkusa.

    • Administrative, technical, or logistic support: K. Fujiki, I. Takashimizu, J. Kumagai, T. Tanizawa, Y. Eishi, T. Yokoyama.

    • Collection and assembly of data: T. Ohkusa.

    Summary for Patients

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