Salvage Treatment with Boceprevir-based Triple Therapy after Failed Treatment of Acute Hepatitis C with Dual Therapy: Presidential Poster

Abstract

Purpose: Acute hepatitis C virus (HCV) infection is usually defined by the presence of signs or symptoms of hepatitis within six months of presumed HCV exposure. While the majority of patients with acute HCV infection are asymptomatic, some do present with symptoms. Treatment of acute HCV infection with interferon is recommended in patients who do not spontaneously clear the virus within 12 weeks of diagnosis, and the vast majority of patients (>80%) who are treated will have a sustained virologic response (SVR) with interferon alone. Recommendations are lacking, however, for patients who do not respond well to standard treatment of acute hepatitis C, and at this time, the use of protease inhibitors in the treatment of acute HCV infection is not widely advocated. We present a case of acute HCV infection that was treated with boceprevir-based triple therapy after failure of treatment with combined pegylated interferon and ribavarin. A 24-year-old female was admitted to the hospital with abdominal pain, vomiting and jaundice. Her transaminases were elevated, with ALT 673 and AST 971. Work-up revealed positive HCV antibodies, with HCV RNA viral load of 3.1 million copies and genotype 1b. The patient had been hospitalized one month prior, and HCV antibodies were negative at the time, indicating a recent infection consistent with acute hepatitis C. Follow-up eight weeks after diagnosis revealed HCV RNA of 5760 copies, with hopes that the patient would spontaneously clear the virus by 12 weeks. However, the HCV RNA viral load increased to 165,160 copies at 12 weeks, and the patient was started on treatment with combined pegylated interferon and ribavarin. The patient failed to respond, however, and after 12 weeks of dual therapy, her HCV RNA had actually increased to 327,000 copies. At this point, given the evident lack of response to combined pegylated interferon and ribavirin, it was decided to add a protease inhibitor, and boceprevir was added without an interruption in therapy, with plans to treat with triple therapy for an additional 44 weeks. Four weeks after the addition of boceprevir, the patient's HCV RNA viral load was undetectable and has remained undetectable at end of treatment (pending SVR). As this case illustrates, immediate initiation of protease inhibitor-based triple therapy may be a reasonable treatment option in patients with acute genotype 1 HCV infection who do not respond to standard therapy. Studies are needed to better determine the efficacy and optimal duration of treatment in this patient population.