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BACKGROUND:Erythropoietin (EPO) not only stimulates erythropoiesis but alsothrombopoiesis. As pegylated-interferon-alpha(PEG-IFN-alpha)-inducedthrombocytopenia may become a limiting factor for continuation of therapy, thepresent study investigated if EPO can alleviate PEG-IFN-alpha inducedthrombocytopenia. Further, we hypothesize that EPO increases platelet reactivityand protease activated receptor 1 (PAR-1) expression during combinationantiviral therapy. METHODS: Forty patients with chronic hepatitis C receivedeither 10,000 IU EPO 3 x/week or placebo in a randomized, placebo-controlled,double-blinded fashion for 4 wk and combination antiviral therapy withPEG-IFN-2a and ribavirin. RESULTS: EPO alleviated the decrease in hemoglobinduring combination antiviral therapy with ribavirin (10%vs 20%, p < 0.0001).Platelet counts decreased stronger in EPO than in placebo group on day 28 (p=0.007). EPO induced a 40% increase in PAR-1 (p < 0.0001), which wasaccompanied by 100% increase in platelet reactivity (p < 0.0001). PFA-100platelet plug formation time and PEG-IFN-alpha-induced vWF-increase were notdifferent between study groups. CONCLUSIONS: Treatment with EPO alleviated thedecrease in hemoglobin but worsened PEG-IFN-alpha induced thrombocytopeniaafter the first 4 wk of combination therapy. EPO caused PAR-1 receptorupregulation on platelets, which promoted an increase in platelet reactivitywithout affecting PFA-100 platelet plug formation time. EPO is not a usefuloption for short-term support of platelet production during antiviral therapy. Leggil'articolo