Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation

It has been suggested that hepatitis C virus (HCV) infection could be assoc iated with B-cell clonal expansion. The aim of this study was to analyze th e relationship between lymphoproliferative disorders and HCV infection in l iver transplant recipients. We studied 157 patients receiving a liver trans plant between January 1989 and May 1997 with a follow-up longer than 3 mont hs. The incidence of posttransplant lymphoproliferative disorders (PTLDs) w as analyzed with reference to the indication for liver transplantation, the induction and maintenance immunosuppression, the incidence of acute reject ion episodes, and Epstein-Barr virus (EBV) infection. Six PTLDs occurred af ter a median posttransplant follow-up of 7 months (3.8%). Four of the 6 PTL Ds occurred among the 38 patients transplanted for HCV-related cirrhosis, a nd 2 PTLDs occurred in the 119 patients receiving a liver transplant for no n-HCV liver diseases (10.5% vs. 1.7%, respectively; P =.03). The 4-year pro bability of PTLD was significantly higher in patients receiving a liver tra nsplant for HCV-related cirrhosis than non-HCV liver diseases (12.3% vs. 2. 2%, respectively; P =.015). Patients receiving a liver transplant for HCV-r elated cirrhosis were more likely to receive antithymocyte globulins (ATG). However, in patients treated with ATG, the 4-year probability of PTLD was higher among those patients receiving a liver transplant for HCV-related ci rrhosis than for non-HCV liver diseases (27.1% vs. 6.4%, respectively; P =. 08). EBV gene products were detected in tumor tissues in 3 of 4 patients wi th HCV-associated PTLD. Our data suggest that, in addition to EBV infection , 2 mutually nonexclusive factors, i.e., the use of ATG and HCV infection, could play a role in the occurrence of PTLD after a liver transplant for HC V-related cirrhosis.