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Original Article |
1 Department of Epidemiology and Public Health, Imperial College London;
2 Division of Clinical Epidemiology, German Cancer Research Centre, Heidelberg, Germany;
3 Institute of Pathology, University of Würzburg, Würzburg, Germany;
4 Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark;
5 Department of Haematology, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark
6 Department of Clinical Epidemiology, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark;
7 Department of Epidemiology, German Institute of Human Nutrition, Potsdam, Germany;
8 Department of Hygiene and Epidemiology, School of Medicine, University of Athens, Greece;
9 Molecular and Nutritional Epidemiology Unit, CSPO -Scientific Institute of Tuscany, Florence, Italy;
10 Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy;
11 Nutritional Epidemiology Unit, National Cancer Institute, Milan, Italy;
12 Cancer Registry, Azienda Ospedaliera "Civile MP Arezzo", Ragusa, Italy;
13 Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Netherlands;
14 National Institute for Public Health and the Environment, Centre for Nutrition and Health, Bilthoven, The Netherlands;
15 Institute of Community Medicine, University of Tromsø, Tromsø, Norway;
16 Public Health Institute of Navarra, Pamplona, Spain;
17 Epidemiology Department, Murcia Health Council, Spain;
18 Epidemiology Unit, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain;
19 Department of Public Health of Gipuzkoa, San Sebastian, Spain;
20 Public Health Directorate and Health Planning, Asturias, Spain;
21 The Andalusian School of Public Health, Granada, Spain;
22 Department of Public Health and Clinical Medicine, Nutrition. Umeå University, Sweden;
23 Department of Clinical Sciences, Malmö University Hospital, Malmö, Sweden;
24 Dept. of Surgery, Malmö University Hospital, Malmö, Sweden;
25 Cancer Research UK, Epidemiology Unit, University of Oxford, UK;
26 MRC Centre for Nutritional Epidemiology in Cancer Prevention and Survival, Department of Public Health and Primary Care, University of Cambridge, UK;
27 Clinical Gerontology, Department of Public Health and Primary Care, University of Cambridge, UK;
28 Nutrition and Hormones Group, International Agency for Research on Cancer, Lyon, France;
29 Gene-Environment Epidemiology Group, International Agency for Research on Cancer, Lyon, France
Correspondence: Aneire E. Khan, Department of Epidemiology and Public Health, Division of Epidemiology, Public Health and Primary Care, Imperial College London, St Mary’s Campus, Variety Wing, Norfolk Place, Paddington, London W2 1PG. E-mail:aneire.khan{at}imperial.ac.uk
Background: Non-Hodgkin’s lymphomas are a heterogeneous group of neoplasms arising from the lymphopoietic system including a wide range of subtypes of either B-cell or T-cell lymphomas. The few established risk factors for the development of these neoplasms include viral infections and immunological abnormalities, but their etiology remains largely unknown. Evidence suggests that certain medical conditions may be linked, through immunosuppression, to the risk of non-Hodgkin’s lymphoma. Multiple myeloma is a neoplasm of plasma cells that accounts for approximately 15% of lymphopoietic cancers. Increases in the incidence of non-Hodgkin’s lymphoma and multiple myeloma in the past implicate environmental factors as potential causal agents.
Design and Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC), 1,213 histologically confirmed incident cases of non-Hodgkin’s lymphoma and multiple myeloma (594 men; 619 women) were identified during a follow-up of 8.5 years. Cox proportional hazard models were used to explore the association between self-reported diabetes, diagnosed after 30 years of age, and the risk of non-Hodgkin’s lymphoma overall and multiple myeloma and various lymphoma subtypes.
Results: We found no association between a personal history of diabetes and the risk of non-Hodgkin’s lymphoma overall in men (HR: 1.28, 95% CI: 0.89–1.84), in women (HR: 0.71, 95% CI: 0.41– 1.24), or in men and women combined (HR: 1.09, 95% CI: 0.80–1.47). Among the B-non-Hodgkin’s lymphoma subtypes, we observed a statistically significant increased risk of B-cell chronic lymphocytic leukemia (HR: 2.0, 95% CI: 1.04–3.86) in men, but not in women (HR: 1.07, 95% CI: 0.33–3.43).
Conclusions: This prospective study did not provide evidence for a role of self-reported diabetes in the etiology of non-Hodgkin’s lymphoma overall or multiple myeloma. We found an increased risk of B-cell chronic lymphocytic leukemia among men with diabetes, but not among women. We hypothesize that diabetes may not play a causal role in the etiology of B-cell chronic lymphocytic leukemia, though the underlying pathogenic mechanisms of both disorders may include shared genetic, host and/or environmental susceptibility factors.
Key words: non-Hodgkin’s lymphoma, diabetes, cohort study.
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