Studies on Platelets

cytopetsia its the peripheral blood with tsormal or itscreased numbers of megakaryocytes its the bone marrow has beets explaitsed by a number of theories which are sharply cotstrastiisg. As poitsted out by Hayem,’ the fitsditsgs its the disease could l)e explaitsed equally well on the basis of either a defect of platelet formatiots or of an excessive disposal or destructioti of platelets in the peripheral circulatiots or its peripheral orgatss. Several mechanisms have beets itsvoked to explaits either possibility. Fraisk attributed the thrombocytopetsia of I.T.P. to decreased formatiots of platelets by the megakaryocytes,2 probably itshibited in their functioss by tsoxious substances produced its the spleets.3 Dameshek and Miller4 later came to somewhat similar cotsclusiotss from their studies of the megakaryocyte morphology before atsd after spletsectomy. Kaztselsots’s5 suggestiots that removal of the spleets might be valuable was based ous his cotscept that the spleen was a thrombocytolytic organ. Doats atsd his collaborators6 exteisded these ideas with tise cotscept of selective splenic sequestratiots of circulatitsg platelets. Kssowledge of the futsdametstal mechatsisms of the disease has recetstly been advanced through a number of sigtsificant observatiotss: (1) elucidatiots of the mechanism of Sedormid7 and Quitsiditse8 purpura; (2) the emphasis oti the frequtetst coexistence of I.T.P. atsd acquired hemolytic atsemia ; “ (3) the thrombocytopetsic activity of plasma from itsdividuals with I.T.P. whets itijected itsto