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Reply to: Sustained resolutin of fibrosing cholestatic hepatitis C despite viremic relapse after stopping pegylated interferon and ribavirin therapy

We wish to thank Dr. Hayashi and colleagues for their interest in our cholestatic hepatitis C virus (HCV) series and their case report. This also provides an opportunity for additional data on the patient with the shortest follow-up in our series (patient 7) who underwent primary liver transplantation in 2001. Patient 7 was HCV RNA–negative when he moved and stopped antiviral therapy in January 2004, 33 months after initiating combination therapy. Thirteen months later, he presented with a total bilirubin of 9.0 (peaking at 11.0) and aspartate aminotransferase and alanine aminotransferase levels of 540 and 668, respectively. Liver biopsy confirmed cholestatic HCV and no evidence of rejection. He was reinitiated on pegylated interferon but failed to have a virologic response (total bilirubin, 2.6 mg/dL; aspartate aminotransferase, 99; and alanine aminotransferase, 117; as of May 2006). Hayashi and colleagues describe a patient with cholestatic HCV (peak total bilirubin, 12.3 mg/dL) who received 38 weeks of antiviral therapy with pegylated interferon and ribavirin. This resulted in transient clearance of viremia and lack of immediate graft failure. We would temper the enthusiasm of a “successful outcome” with recognition that the patient has evidence of advanced fibrosis (at least bridging), high-level viremia, and an extremely high likelihood of developing allograft cirrhosis (if not already present) and its attendant complications in the next few years. While their interventions likely changed the course of cholestatic HCV, it is worth noting that back in 1998, we observed that patients with significant hyperbilirubinemia ( 3.5 mg/dL) attributable exclusively to HCV recurrence can experience spontaneous normalization of their serum bilirubin and aminotransferases (without antiviral therapy) over an average of 8 months. Invariably, however, these patients developed allograft cirrhosis. It is certainly possible that the pegylated form of interferon is better able to prevent the sudden relapse of rebound hyperbilirubinemia we observed in most of our cholestatic patients initially treated with nonpegylated interferon, but this remains a speculation. It is also important to consider the antifibrotic benefits of sirolimus and agree with its usage in this case. Clearly, this patient warrants close monitoring and protocol biopsies at least every year. Based on our experience and the fact he has already developed advanced fibrosis, we would continue antiviral therapy, titrating according to side effects and targeting nondetectable viremia, because of the very high risk of HCVrelated allograft failure.