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Blood, 15 December 2007, Vol. 110, No. 13, pp. 4599-4605.
Prepublished online as a Blood First Edition Paper on September 12, 2007; DOI 10.1182/blood-2007-07-101956.


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Submitted July 19, 2007
Accepted September 9, 2007

Hepatitis C virus infection and risk of post-transplant lymphoproliferative disorder among solid organ transplant recipients

Lindsay M Morton*, Ola Landgren, Nilanjan Chatterjee, David Castenson, Ruth Parsons, Robert N Hoover, and Eric A Engels

Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, United States
Information Management Services, Inc., Rockville, MD, United States

* Corresponding author; email: mortonli{at}mail.nih.gov.

Post-transplant lymphoproliferative disorder (PTLD) is a serious complication of solid organ transplantation. Hepatitis C virus (HCV) infection has been linked to increased risk of lymphoma among immunocompetent individuals. We therefore investigated the association between HCV infection and PTLD in a retrospective cohort study of all individuals in the US who received their first solid organ transplant during 1994- 2005 (N=210,763), using Scientific Registry of Transplant Recipients data. During follow-up, 1630 PTLD cases were diagnosed. HCV prevalence at transplant was 11.3%. HCV infection did not increase PTLD risk in the total cohort (Cox regression model, hazard ratio (HR)=0.84, 95% confidence interval (CI) 0.68-1.05), even after adjustment for type of organ transplanted, indication for transplant, degree of HLA mismatch, donor type, or use of immunosuppression medications. Additional analyses also revealed no association by PTLD subtype (defined by site, pathology, cell type, and tumor EBV status). HCV infection did increase PTLD risk among the 2.8% of patients (N=5959) who were not reported to have received immunosuppression maintenance medications prior to hospital discharge (HR=3.09, 95%CI 1.14-8.42; p-interaction=0.007). Our findings suggest that HCV is not a major risk factor for PTLD, which is consistent with the model in which an intact immune system is necessary for development of HCV-related lymphoproliferation.


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