Gilbert’s syndrome and antiviral therapy of hepatitis C
Journal Title: Annals of Hepatology - Year 2009, Vol 8, Issue 3
Abstract
Treatment of chronic hepatitis C with type I interferons and ribavirin can be associated with exacerbation of hepatitis and sometimes liver decompensation. We report two patients with chronic hepatitis C virus infection who experienced a severe increase of bilirubin levels of up to 17 times upper the limit of normal value in the absence of deterioration of hepatic function during therapy with pegylated-interferon and ribavirin. A genetic disposition for Gilbert’s syndrome explained the adverse events and permitted a continuation of therapy leading to a sustained clearance of chronic hepatitis C infection. Since one patient jaundiced already during a lead-in treatment period with ribavirin monotherapy we suggest that hyperbilirubinaemia during combination therapy is primarily caused by ribavirin rather than by effects of interferon alpha on DP-glucuronosyltransferase activities. Of note, both patients recovered from their initial unconjugated hyperbilirubinemia despite continuation of ribavirin therapy, which indicates that compensatory mechanisms leading to a normalization of UGT1A1 activity are likely.
Authors and Affiliations
Katja Deterding, Kurt Grüngreiff, Tim Lankisch, Andrej Potthoff, Matthias Bahr, Michael Manns, Heiner Wedemeyer, Christian Strassburg
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IN MEMORIAM-Professor Andrew Burroughs
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