Premium
Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation
Author(s) -
Hézode Christophe,
Duvoux Christophe,
Germanidis Georgios,
RoudotThoraval Françoise,
Vincens AnneLaure,
Gaulard Philippe,
Cherqui Daniel,
Pawlotsky JeanMichel,
Dhumeaux Daniel
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510300314
Subject(s) - medicine , lymphoproliferative disorders , immunosuppression , cirrhosis , liver transplantation , hepatitis c virus , gastroenterology , hepatitis c , incidence (geometry) , transplantation , immunology , virus , lymphoma , physics , optics
It has been suggested that hepatitis C virus (HCV) infection could be associated with B‐cell clonal expansion. The aim of this study was to analyze the relationship between lymphoproliferative disorders and HCV infection in liver transplant recipients. We studied 157 patients receiving a liver transplant between January 1989 and May 1997 with a follow‐up longer than 3 months. The incidence of posttransplant lymphoproliferative disorders (PTLDs) was analyzed with reference to the indication for liver transplantation, the induction and maintenance immunosuppression, the incidence of acute rejection episodes, and Epstein‐Barr virus (EBV) infection. Six PTLDs occurred after a median posttransplant follow‐up of 7 months (3.8%). Four of the 6 PTLDs occurred among the 38 patients transplanted for HCV‐related cirrhosis, and 2 PTLDs occurred in the 119 patients receiving a liver transplant for non‐HCV liver diseases (10.5% vs. 1.7%, respectively; P = .03).The 4‐year probability of PTLD was significantly higher in patients receiving a liver transplant for HCV‐related cirrhosis than non‐HCV liver diseases (12.3% vs. 2.2%, respectively; P = .015). Patients receiving a liver transplant for HCV‐related 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 cirrhosis 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 with 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 HCV‐related cirrhosis.