ROLE OF COMPLEMENT IN IMMUNE OR IDIOPATHIC THROMBOCYTOPENIC PURPURA

The clinical course of immune or idiopathic thrombocytopenic purpura ( ITP) is variable, suggesting different mechanisms for the decreased pl atelet count. The complement factors C3 and C4 have been detected on p latelets, both alone and in association with immunoglobulin G (IgG), a nd a reduced platelet survival time has been described. Platelets have the capacity to interact with the complement system since they have b oth complement receptors and complement regulatory proteins on their c ell membranes. The membrane attack complex (C5b-9) induced by antiplat elet antibodies generates platelet microparticles in a concentration-d ependent manner. A marked variation in resistance to this phenomenon h as been demonstrated between individuals and between men and women. Th ese platelet microparticles seem to retain their biological role in ha emostasis. Platelets also appear to play a role in the processing of i mmune complexes. Immunoglobulins and complement factors are found in s everal clinical situations where circulating immune complexes are expe cted. Furthermore, human platelets bind immune complexes in vitro and the reaction can be blocked by antireceptor antibodies to immunoglobul ins and complement. These findings raise a number of questions about t he role of complement in the pathophysiology of ITP.