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Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and hepatocellular carcinoma (HCC). Chronic HCV infection accounts for more than 75% of cirrhosis and end-stage liver disease worldwide. Even though recent anti-HCV treatment has resulted in improved clinical outcomes, HCV-related mortality remains at 4% per annum. Anti-HCV therapy has been complicated by a high rate of side effects and a low barrier to resistance. Telaprevir, the most recent protease inhibitor (PI), has been approved in the US.
Case
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A 60-year-old man with a history of HCV-induced cirrhosis and HCC was admitted to the hospital with acute-onset right upper quadrant pain and fever. The pain was sharp and not relieved by rest, and was associated with nausea and vomiting. His liver function tests were elevated: total bilirubin 3.4 mg/dL, ALT 2,202 U/L, AST 830 U/L and alkaline phosphatase 534 U/L. Serological tests confirmed his HCV genotype was 3 and HCV-RNA was 17,137,000 IU/mL. As an inpatient, he received PEG-interferon alfa-2b 180 mcg three times per week for 28 weeks and a dose of telaprevir 500 mg one day prior to completion of the interferon, followed by daily
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