Failure of Intravenous Silibinin Monotherapy to Prevent Hepatitis C Genotype 2A Liver Graft Reinfection
M. et al. Failure of Intravenous Silibinin Monotherapy to Prevent Hepatitis C Genotype 2A Liver Graft Reinfection,
Online ahead of Print
Background: Hepatitis C virus (HCV) recurrence after orthotopic liver transplantation (OLT) remains a serious problem in the clinical management of post-OLT patients. Recently, two case reports have described successful prevention of HCV liver graft reinfection with intravenous silibinin (SIL) monotherapy in two carriers of genotype 3a and 1a/4 HCV. Based on these findings, we decided to offer such a therapy to a 65 year old woman on the OLT list. Case Presentation: A 65 year old patient with HCV 2a cirrhosis, a previous relapse to PegIFN and Rbv therapy, was listed for OLT due to hepatocellular carcinoma. She started SIL monotherapy 24 hours before OLT. After an initial HCV-RNA decline following surgery, a progressive HCV RNA increase was observed. For this reason, SIL was stopped after 15 days of monotherapy. Conclusions: SIL has multiple anti-HCV mechanisms of action, most of them have been characterized in vitro only. Our case report shows that the antiviral effect of SIL might be HCV genotype dependent, as recently suggested by a study, showing no effect of SIL on the HCV-2a subgenomic replicon model. Our case reinforces the need for controlled studies to assess the efficacy of silibinin therapy in HCV infected patients before it can be broadly used in all clinical settings.
Implication for health policy/practice/research/medical education: Silibinin monotherapy is a promising therapeutic option for HCV patients. Our article demonstrates that Silibinin has no effect on genotype 2 HCV, reinforcing the need for controlled studies on this drug before it can be routinely used in clinical practice. Please cite this paper as: Aghemo A, Bhoori S, De Nicola S, Mazzaferro V, Colombo M. Failure of Intravenous Silibinin Monotherapy to Prevent Hepatitis C Genotype 2A Liver Graft Reinfection. Hepat Mon. 2012;12(6): 411-4. DOI: 10.5812/hepatmon.6135
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