Anemia and clinical outcomes in hepatitis C

Abstract

Combination therapy with pegylated interferon and ribavirin is currently the most effective treatment for chronic hepatitis C (CHC), and rates of sustained virological response (SVR) now exceed 50% [1,2]. Yet as SVR rates have increased, so have rates of treatmentrelated anemia. Anemia is a common consequence of antiviral treatment for CHC and may occur in as many as half of all treated patients [3–5]. In two recent clinical trials, dose reductions due to anemia occurred in 0–3% of patients treated with 48 weeks of standard or pegylated interferon monotherapy, in up to 19% of patients treated with a combination of standard interferon and ribavirin, and in up to 22% of patients treated with pegylated interferon and ribavirin [1,2]. Dose reductions have also been demonstrated in as many as 36% of patients treated with pegylated interferon and ribavirin in a clinical practice setting [6]. Both standard and pegylated interferon have been shown to cause mild anemia, mediated by bone marrow suppression, and may reduce hemoglobin concentrations by at least 2 g/dL in approximately 25–30% of patients [4,5]. Ribavirin is associated with a welldescribed, dose-dependent hemolytic anemia that leads to hemoglobin decreases of at least 2 g/dL in as many as 80% of patients and maximum decreases of at least 4 g/dL in as many as 20% of patients [7]. This anemia is mediated by the transport of ribavirin into the erythrocyte, which does not contain the phosphatases necessary to hydrolyze ribavirin metabolites. These