The efficacy of HCV therapy has improved dramatically with the advent of PEG/RBV. In some patients with HCV, however, its effectiveness and safety are limited by the development of significant hematologic complications, including neutropenia, anemia, and thrombocytopenia. The mechanisms of these adverse effects of HCV therapy are understood reasonably well, and are largely attributable to IFN-related bone marrow suppression along all three cell lines and RBV-related hemolytic anemia. In studies, clinical events (eg, serious infection, hemorrhage) related to the development of cytopenias have been reported rarely; however, fatigue and decreased QOL caused by anemia are common and may contribute to nonadherence to treatment and its early discontinuation. Furthermore, cytopenias are one of the most common reasons for dose reduction of PEG or RBV or both, and these may limit the effectiveness of treatment. Although dose reduction is an effective strategy to stabilize or correct treatment-related cytopenias, growth factors also have a role in their management. The correction of anemia with epoetin alfa is supported by randomized, controlled trials that demonstrate the epoetin alfa may increase Hb, maintain RBV dose, and improve QOL in such patients. In contrast, data to support use of filgrastim and IL-11 largely are extrapolated from clinical data from oncology. Further research is needed to define the role of these agents for managing HCV treatment-related cytopenias and to assess the impact of epoetin alfa on HCV virologic outcomes.
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