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Original Article
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Volume 330:1267-1271 May 5, 1994 Number 18
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Helicobacter pylori Infection and Gastric Lymphoma
Julie Parsonnet, Svein Hansen, Larissa Rodriguez, Arnold B. Gelb, Roger A. Warnke, Egil Jellum, Norman Orentreich, Joseph H. Vogelman, and Gary D. Friedman

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ABSTRACT

Background Helicobacter pylori infection is a risk factor for gastric adenocarcinoma. We examined whether this infection is also a risk factor for primary gastric non-Hodgkin's lymphoma.

Methods This nested case-control study involved two large cohorts (230,593 participants). Serum had been collected from cohort members and stored, and all subjects were followed for cancer. Thirty-three patients with gastric non-Hodgkin's lymphoma were identified, and each was matched to four controls according to cohort, age, sex, and date of serum collection. For comparison, 31 patients with nongastric non-Hodgkin's lymphoma from one of the cohorts were evaluated, each of whom had been previously matched to 2 controls. Pathological reports and specimens were reviewed to confirm the histologic type of the tumor. Serum samples from all subjects were tested for H. pylori IgG by an enzyme-linked immunosorbent assay.

Results Thirty-three cases of gastric non-Hodgkin's lymphoma occurred a median of 14 years after serum collection. Patients with gastric lymphoma were significantly more likely than matched controls to have evidence of previous H. pylori infection (matched odds ratio, 6.3; 95 percent confidence interval, 2.0 to 19.9). The results were similar in both cohorts. Among the 31 patients with nongastric lymphoma, a median of six years had elapsed between serum collection and the development of disease. No association was found between nongastric non-Hodgkin's lymphoma and previous H. pylori infection (matched odds ratio, 1.2; 95 percent confidence interval, 0.5 to 3.0).

Conclusions Non-Hodgkin's lymphoma affecting the stomach, but not other sites, is associated with previous H. pylori infection. A causative role for the organism is plausible, but remains unproved.


Source Information

From the Departments of Medicine and Health Research and Policy (J.P., L.R.) and the Department of Pathology (A.B.G., R.A.W.), Stanford University School of Medicine, Stanford, Calif.; the Cancer Registry of Norway, Oslo (S.H.); the Janus Committee, Norwegian Cancer Society, Oslo (E.J.); the Orentreich Foundation for the Advancement of Science, Cold Spring, N.Y. (N.O., J.H.V.); and the Division of Research, Kaiser Permanente Medical Care Program, Oakland, Calif. (G.D.F.).

Address reprint requests to Dr. Parsonnet at HRP Bldg., Rm. 225, Stanford University, Stanford, CA 94305.

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