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Sustained eradication of hepatitis C virus by low-dose long-term interferon therapy in a renal transplant recipient with dual infection with hepatitis B and C viruses: a case report

DOI: 10.1186/1752-1947-5-246

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Abstract:

In this article, we report the case of a 51-year-old Taiwanese man with dual infection with HBV and HCV prior to renal transplantation. Low-dose interferon (3 to 6 × 106 U/week) and ribavirin (100 mg/day to 200 mg/day) were prescribed following the reactivation of the man's HCV after renal transplantation. Additionally, lamivudine (100 mg/day) was administered concomitantly to prevent HBV reactivation. His initial serum HCV RNA concentration was 5.2 × 106 copies/mL (genotype 2a). After three and one-half years of antiviral therapy, his HCV was successfully eradicated without any episodes of allograft rejection. His serum HCV RNA remained negative six months after withdrawal from interferon and ribavirin treatment. His serum HBV DNA remained undetectable throughout the course of therapy.Low-dose, long-term interferon therapy may achieve sustained eradication of HCV in the renal transplant recipient with dual infection with HBV and HCV.Chronic hepatitis C virus (HCV) infection may lead to severe sequels such as liver cirrhosis and hepatoma [1]. It was recognized as an important cause of morbidity and mortality in renal transplant recipients [2]. Besides accelerated deterioration of liver function in chronic HCV infection, HCV-related glomerulopathy [3] and HCV-associated fibrosing cholestatic hepatitis [4] have also been documented in renal transplant recipients. Although interferon plus ribavirin combination therapy has been established as the standard treatment for chronic HCV infection, the risk of acute rejection associated with interferon administration has greatly hindered the use of this treatment [5]. In an area where chronic hepatitis B virus (HBV) infection is prevalent, such as Asia, the challenge is even greater, because dual infection with HBV and HCV may be encountered. Mutual interference of HCV and HBV replication has been reported in many studies with alternately dominant hepatitis activities caused by HBV and HCV [6]. More severe liver diseases have

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