Treatment options in the management of thrombocytopenia in patients infected with HCV

Abstract

) inpatients with chronic hepatitis has been associated with twofactors: the first is hypersplenism resulting from splenomegalyin portal hypertension [1]. The spleen continuouslysequesters one-third of circulating platelets, so thatsplenomegaly increases the fraction of platelets trapped inthe splenic sinusoids, especially when resulting from passivecongestion or an increase in venous portal pressure [1].Hypersplenism seems to be the most common cause ofthrombocytopenia associated with liver cirrhosis and portalhypertension.The second mechanism is related to the decreasedproduction of thrombopoietin, a hormone produced byhepatocytes, which regulates the development of themegakaryocyte. In cirrhosis, due to the reduction in the massof functioning hepatocytes, there can be a reduction ofthrombopoiesis in the bone marrow, leading tothrombocytopenia in the peripheral blood [1].In some situations, patients who are otherwise eligible forHCV treatment with interferon and ribavirin cannot be sotreated because their platelets counts are low, whichjeopardizes the treatment [2,3].Nevertheless, hepatitis C patients treated with interferon andribavirin also present a drop in the platelet count as a sideeffect [2,3].There is as yet no treatment consensus in the literature forthe management of these patients. We therefore present somerelated studies that address the management of these patients,in the pre-treatment and intra-treatment phases.Patients receiving interferon alpha or peginterferon alphacan present a 30-50% reduction in the baseline platelet count,and a dose reduction is necessary in approximately 4% of thepatients [2,3]. We should consider possible reduction of thedose when platelet counts drop to < 50,000/mm