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Hepatitis C Virus & Risk of Non-Hodgkin's Lymphoma

Hepatitis C Virus and Risk of Non-Hodgkin Lymphoma: A Population-Based Case-Control Study among Connecticut Women

Lindsay McOmber Morton1, Eric A. Engels4, Theodore R. Holford1, Brian Leaderer1, Yawei Zhang1, Shelia Hoar Zahm4, Peter Boyle3, Bing Zhang5, Stuart Flynn2, Giovanni Tallini2, Patricia H. Owens1 and Tongzhang Zheng1

1 Department of Epidemiology and Public Health and 2 Department of Pathology, Yale University School of Medicine, New Haven, CT; 3 Department of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy; 4 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD; and 5 Department of Epidemiology and Biostatistics, McGill University, Montreal, Canada

Requests for reprints: Tongzhang Zheng, 129 Church Street, Suite 700, New Haven, CT 06510. Phone: (203) 785-2882. E-mail: tongzhang.zheng@yale.edu

Objective: Previous epidemiologic studies of hepatitis C virus (HCV) infection and B-cell non-Hodgkin lymphoma (B-NHL) have yielded conflicting results, perhaps due to differences in the classification of B-NHL and the choice of non-population-based control groups that may not reflect the background population prevalence of HCV.

To further investigate the link between HCV and NHL, we conducted HCV testing on serum samples of 998 women (464 cases; 534 controls) from a population-based case-control study of women in Connecticut.

Methods: Serum samples were screened for HCV antibodies using an enzyme immunoassay; positive samples were confirmed by additional testing for HCV antibodies and for serum HCV RNA.

Results: Approximately 2% (8 of 464) of cases and 1% (5 of 534) of controls tested positive for HCV. The risk of NHL associated with HCV infection appeared to be concentrated among B-cell lymphomas [odds ratio (OR) 2.0; 95% confidence interval (CI) 0.6, 8.2], particularly among follicular lymphomas (OR 4.1, 95% CI 0.8, 19.4).

Conclusion: The primary strength of this study is our use of a population-based study design, although the low prevalence of HCV among women in Connecticut resulted in wide CIs for the estimated association between HCV and B-NHL subtypes.

Our study suggests that HCV may be associated with increased risk of development of B-NHL, and that this risk may vary by B-NHL subtype among women.

Due to the relatively low prevalence of HCV in our study population and the scarcity of population-based epidemiological research on this subject, our study highlights the need for additional large, population-based studies of the role of HCV in the etiology of B-NHL.

Cancer Epidemiology Biomarkers & Prevention Vol. 13, 425-430, March 2004


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