Investigation of megakaryocytes apoptosis in children with acute and chronic idiopathic thrombocytopenic

Idiopathic thrombocytopenic purpura (ITP) is one of the most frequent causes of thrombocytopenia in children. The cause of thrombocytopenia in ITP is the premature destruction of platelets. The widely accepted essential pathophysiological mechanism for ITP is the development of autoantibodies directed against the platelet surface. These antibody-coated circulating platelets are then recognised by the Fc receptor on the splenic macrophages which ingest and destroy them. However, with the available technological methods, anti-platelet antibodies remain undetermined at least for the 20% of ITP cases. Therefore, different mechanisms may play a role in the pathophysiology of ITP. Several studies have been performed with an aim to search the possible mechanisms. Recently, bone marrow studies in patients with ITP demonstrated ineffective megakaryopoiesis and arrest of maturation in megakaryocytes. The aim of this study was to investigate megakaryocyte apoptosis in bone marrow of children with acute and chronic ITP and the role of apoptosis in ITP pathophysiology. This study was performed between September 1, 2000 and August 1, 2001, Fifteen children with acute ITP and 10 children with chronic ITP were included. Ten children with skolyosis who have been healthy otherwise were studied to serve as a control group. Medical histories, physical examination findings and periferic blood findings of patients were recorded. In all children, megakaryocytes were isolated from bone marrow samples using CD61+ magnetic beads and megakaryocyte apoptosis was studied with TUNEL method. In our study, the ratio of megakaryocyte apoptosis in patients with chronic ITP was significantly lower than the cases with acute ITP (p=0.030). This result suggested that the pathogenic mechanism for acute and chronic ITP may be different. Further studies with a larger patient population should be performed to determine the reason for decreased megakaryocyte apoptosis in pediatric patients with chronic ITP. These future studies may also help to clarify the pathogenic mechanisms for the development of chronic ITP. 51