BackgroundHelicobacter pylori infection plays an importantpart in the development of atrophic gastritis and intestinalmetaplasia, conditions that predispose patients to gastric cancer.Profound suppression of gastric acid is associated with increasedseverity of gastritis caused by H. pylori, but it is not knownwhether acid suppression increases the risk of atrophic gastritis.
Methods We studied patients from two separate cohorts who werebeing treated for reflux esophagitis: 72 patients treated withfundoplication in Sweden and 105 treated with omeprazole (20to 40 mg once daily) in the Netherlands. In both cohorts, thepatients were followed for an average of five years (range,three to eight). After fundoplication, the patients did notreceive acid-suppressive therapy. The presence of H. pyloriwas assessed at the first visit by histologic evaluation inthe fundoplication group and by histologic and serologic evaluationin the omeprazole group. The patients were not treated for H.pylori infection. Before treatment and during follow-up, thepatients underwent repeated gastroscopy, with biopsy samplingfor histologic evaluation.
Results Among the patients treated with fundoplication, atrophicgastritis did not develop in any of the 31 who were infectedwith H. pylori at base line or the 41 who were not infected;1 patient infected with H. pylori had atrophic gastritis beforetreatment that persisted after treatment. Among the patientstreated with omeprazole, none of whom had atrophic gastritisat base line, atrophic gastritis developed in 18 of the 59 infectedwith 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 infectionwho are treated with omeprazole are at increased risk of atrophicgastritis.
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 1417, 1995.
Address reprint requests to Dr. Kuipers at the Department of Gastroenterology, Free University Hospital, P.O. Box 7057, 1007 MB Amsterdam, the Netherlands.
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