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Blood, 15 June 2008, Vol. 111, No. 12, pp. 5524-5529.
Prepublished online as a Blood First Edition Paper on April 18, 2008; DOI 10.1182/blood-2007-08-109611.


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CLINICAL TRIALS AND OBSERVATIONS

Borrelia infection and risk of non-Hodgkin lymphoma

Claudia Schöllkopf1, Mads Melbye1, Lars Munksgaard2, Karin Ekström Smedby3, Klaus Rostgaard1, Bengt Glimelius4,5, Ellen T. Chang6,7, Göran Roos8, Mads Hansen2, Hans-Olov Adami3,9, and Henrik Hjalgrim1

1 Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark; 2 Department of Hematology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; 3 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; 4 Department of Pathology and Oncology, Karolinska Institutet, Stockholm, Sweden; 5 Department of Oncology, Radiology and Clinical Immunology, Uppsala University, Uppsala, Sweden; 6 Northern California Cancer Center, Fremont; 7 Department of Health Research and Policy, Stanford University School of Medicine, CA; 8 Department of Pathology, Norrlands University Hospital, Umeå, Sweden; and 9 Department of Epidemiology, Harvard School of Public Health, Boston, MA

Reports of the presence of Borrelia burgdorferi DNA in malignant lymphomas have raised the hypothesis that infection with B burgdorferi may be causally related to non-Hodgkin lymphoma (NHL) development. We conducted a Danish-Swedish case-control study including 3055 NHL patients and 3187 population controls. History of tick bite or Borrelia infection was ascertained through structured telephone interviews and through enzyme-linked immunosorbent assay serum analyses for antibodies against B burgdorferi in a subset of 1579 patients and 1358 controls. Statistical associations with risk of NHL, including histologic subtypes, were assessed by logistic regression. Overall risk of NHL was not associated with self-reported history of tick bite (odds ratio [OR] = 1.0; 95% confidence interval: 0.9-1.1), Borrelia infection (OR = 1.3 [0.96-1.8]) or the presence of anti-Borrelia antibodies (OR = 1.3 [0.9-2.0]). However, in analyses of NHL subtypes, self-reported history of B burgdorferi infection (OR = 2.5 [1.2-5.1]) and seropositivity for anti-Borrelia antibodies (OR = 3.6 [1.8-7.4]) were both associated with risk of mantle cell lymphoma. Notably, this specific association was also observed in persons who did not recall Borrelia infection yet tested positive for anti-Borrelia antibodies (OR = 4.2 [2.0-8.9]). Our observations suggest a previously unreported association between B burgdorferi infection and risk of mantle cell lymphoma.


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