Antiviral therapy for recurrent hepatitis C in liver transplantation has been associated with the development of chronic rejection. The aim of this study was to assess the incidence, evolution, and risk factors associated with the development of chronic rejection during posttransplant hepatitis C virus antiviral therapy. Seventy-nine patients with posttransplant recurrent hepatitis C who were treated with pegylated interferon and ribavirin were prospectively followed. Liver biopsy was performed before antiviral therapy was initiated and when liver tests worsened during therapy. Pretransplant and posttransplant factors were analyzed as potential risk factors for the development of chronic rejection. Seven of 79 patients (9%) developed chronic rejection during antiviral therapy. The mean time from the start of treatment to the development of chronic rejection was 5.8 months (3-12 months). An analysis of factors associated with the development of chronic rejection showed that the use of cyclosporine as immunosuppression therapy (6 of 19 patients who received cyclosporine developed chronic rejection in comparison with only 1 of 57 patients who received tacrolimus; P ϭ 0.0013), achievement of sustained virological response (P ϭ 0.043), and ribavirin discontinuation (P ϭ 0.027) were associated with the development of chronic rejection. In conclusion, the development of chronic rejection during posttransplant pegylated interferon and ribavirin therapy is a severe complication. The use of cyclosporine, ribavirin discontinuation, and viral infection elimination seem to be associated with the development of this complication. End-stage liver disease due to hepatitis C virus (HCV) is currently the leading indication for liver transplantation (LT) worldwide. HCV recurrence after transplantation is almost universal, and most patients will develop chronic hepatitis of the graft during follow-up.1 In LT recipients, chronic HCV infection leads to cirrhosis in up to 30% of patients in the first 5 years after LT, and many of these patients will experience clinical decompensation within 1 year after the diagnosis.2,3 Indeed, the main cause of death in HCV transplant recipients is allograft failure due to HCV recurrence. 1,4 At the present time, interferon (IFN)-based therapy is the only available treatment strategy to achieve viral clearance and to stop disease progression. Currently, the mainstay of posttransplant HCV hepatitis therapy is a combination of pegylated interferon (PEG-IFN) and ribavirin. This therapy has been demonstrated to produce a sustained virological response (SVR) in 21% to 50% of patients, 5-10 and it has been associated with improvements in liver histology and long-term outcome. 11,12 However, the use of antiviral therapy after LT is limited by poor tolerability and adverse effects. A poten-
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