A CHANGE in the concepts regarding idiopathic thrombocytopenic purpura has occurred during the past fifteen years mainly because of the recognition of three important facts: The thrombocytopenia is the result of increased platelet destruction. The old hypothesis, originally postulated by Frank,1 , 2 of a toxic depression of megakaryocytes and their activity resulting in thrombocytopenia has been disproved since a shortened platelet life-span has regularly been found in the disease. An antiplatelet factor with characteristics of an antibody is present in the plasma of these patients.3 In fact, normal donor platelets infused into the patient are destroyed as rapidly as . . .