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Original Article
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Volume 334:1018-1022 April 18, 1996 Number 16
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Atrophic Gastritis and Helicobacter pylori Infection in Patients with Reflux Esophagitis Treated with Omeprazole or Fundoplication
Ernst J. Kuipers, M.D., Ph.D., Lars Lundell, M.D., Ph.D., Elly C. Klinkenberg-Knol, M.D., Ph.D., Niilo Havu, M.D., Ph.D., Henk P.M. Festen, M.D., Ph.D., Bengt Liedman, M.D., Ph.D., Cornelius B.H.W. Lamers, M.D., Ph.D., Jan B.M.J. Jansen, M.D., Ph.D., Jan Dalenbäck, M.D., Ph.D., Pleun Snel, M.D., Ph.D., G. Frits Nelis, M.D., Ph.D., and Stephan G.M. Meuwissen, M.D., Ph.D.

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ABSTRACT

Background Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients to gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis.

Methods We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation.

Results Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori (P<0.001) and 2 of the 46 who were not infected (P = 0.62).

Conclusions Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.


Source Information

From the Departments of Gastroenterology of the Free University Hospital, Amsterdam (E.J.K., E.C.K.-K., H.P.M.F., S.G.M.M.), University Hospital, Leiden (C.B.H.W.L.), University Hospital, Nijmegen (J.B.M.J.J.), Slotervaart Hospital, Amsterdam (P.S.), and Sophia Hospital, Zwolle (G.F.N.) — all in the Netherlands; the Department of Surgery, Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden (L.L., B.L., J.D.); and Astra, Södertälje, Sweden (N.H.). Presented in part at the annual meeting of the American Gastroenterology Association, San Diego, Calif., May 14–17, 1995.

Address reprint requests to Dr. Kuipers at the Department of Gastroenterology, Free University Hospital, P.O. Box 7057, 1007 MB Amsterdam, the Netherlands.

Full Text of this Article


Related Letters:

Atrophic Gastritis and Helicobacter pylori in Reflux Esophagitis
Repucci A. H., Kuipers E. J., Klinkenberg-Knol E., Meuwissen S. G.M., Lundell L.
Extract | Full Text  
N Engl J Med 1996; 335:750-751, Sep 5, 1996. Correspondence

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