Volume 30, Issue 3 pp. 775-778
Original Article
Free Access

Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation

Christophe Hézode M.D.

Corresponding Author

Christophe Hézode M.D.

Departments of Hepatology-Gastroenterology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

Service d'Hépatologie et de Gastroentérologie, Hôpital Henri Mondor, 51 avenue du maréchal de-Lattre-de-Tassigny, 94010 Créteil, France. fax: (33) 1 49 81 2352===Search for more papers by this author
Christophe Duvoux

Christophe Duvoux

Departments of Hepatology-Gastroenterology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Georgios Germanidis

Georgios Germanidis

Virology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Françoise Roudot-Thoraval

Françoise Roudot-Thoraval

Public Health, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Anne-Laure Vincens

Anne-Laure Vincens

Departments of Hepatology-Gastroenterology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Philippe Gaulard

Philippe Gaulard

Pathology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Daniel Cherqui

Daniel Cherqui

Surgery, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Jean-Michel Pawlotsky

Jean-Michel Pawlotsky

Virology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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Daniel Dhumeaux

Daniel Dhumeaux

Departments of Hepatology-Gastroenterology, Hôpital Henri Mondor, Université Paris XII, Créteil, France

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First published: 30 December 2003
Citations: 60

Abstract

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.

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