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Cancer Epidemiology Biomarkers & Prevention Vol. 13, 944-948, June 2004
© 2004 American Association for Cancer Research

Helicobacter pylori and Malignant Lymphoma in Spain

Silvia de Sanjose1,3, Andrew Dickie4, Tomas Alvaro5, Vicens Romagosa6, Mercedes Garcia Villanueva7, Eva Domingo-Domenech1,2, Alberto Fernandez de Sevilla2 and Emad El-Omar4

1 Servei d'Epidemiologia & Registre del Cancer and 2 Hematologia Oncologica, Institut Catala d'Oncologia, Barcelona, Spain; 3 Viral Epidemiology Branch, National Cancer Institute, Bethesda, Maryland; 4 Department of Medicine and Therapeutics, Aberdeen University, Scotland; 5 Patologia, Hospital Verge de la Cinta, Tortosa, Spain; 6 Patologia, Ciutat Sanitaria & Universitaria de Bellvitge, Barcelona, Spain; and 7 Patologia, Ramon y Cajal Universidad de Alcala, Madrid, Spain

Requests for reprints:Silvia de Sanjose, Servei d'Epidemiologia & Registre del Cancer, Institut Catala d'Oncologia, Gran Via Km 2.7, 08907 L'Hospitalet, Barcelona, Spain. Phone: (+34)-932607812; Fax: (+34)-932607787. E-mail: s.sanjose{at}ico.scs.es

Helicobacter pylori has been associated with gastric adenocarcinoma and gastric lymphoma. We report on the systematic evaluation of serologic detection of H. pylori in a lymphoma case-control study. Methods: Cases (N = 536) were consecutive patients newly diagnosed with a lymphoid malignancy between 1998 and 2002 in four centers in Spain. Lymphomas were diagnosed and classified using the WHO Classification. Controls (N = 603) were hospitalized patients frequency-matched to the cases by 5-year age group, sex, and study center. Severe immunocompromised patients were excluded as controls. Patients underwent a personal interview and blood sampling. H. pylori infection was evaluated by the presence of IgG antibodies using the Premier enzyme immunoassay kit (Meridian Diagnostics Inc., Cincinnati, OH). Logistic regression analysis was used to estimate the odds ratios and 95% confidence intervals (OR, 95% CI) for lymphoma categories. Results: Anti-H. pylori antibodies were detected in 68.5% of the cases and 71.3% of the controls (P = 0.29) H. pylori was associated with a 3-fold excess risk of splenic marginal B-cell lymphoma (OR = 3.97, 95% CI = 0.92-17.16). H. pylori was not associated with an overall increased risk of extranodal lymphomas (OR = 0.73, 95% CI = 0.44-1.22) but when specific sites were explored, the four mucosa-associated lymphoid tissue and the six diffuse large B-cell lymphomas primary localized in the stomach were all H. pylori seropositive. Conclusion: Persistent infection with H. pylori may be implicated in the development of lymphomas of the gastric mucosa and of the spleen. These results could have clinical implications in the management of splenic marginal zone lymphomas.




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