Interest in thrombocytopenic purpura has recently been stimulated by the demonstration that a circulating thrombocytopenic factor, presumably an antibody, is frequently involved in the pathogenesis of idiopathic thrombocytopenic purpura,1and by the suggestion that platelet transfusions may occasionally provide temporary relief from hemorrhagic manifestations in patients with low platelet levels caused by bone marrow depression.2During the past year, additional evidence has been obtained to indicate the importance of immunologic antiplatelet factors in the production of idiopathic thrombocytopenic purpura. It is the purpose of this paper to review that evidence, to relate it to previous ideas of pathogenesis, and to discuss the possible therapeutic application of platelet transfusions. PATHOGENESIS OF IDIOPATHIC THROMBOCYTOPENIC PURPURA The diminished number of platelets in idiopathic thrombocytopenic purpura has been attributed either to a decrease in their production or to an increased rate of destruction. Frank3was the first investigator to champion the
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Charles C. Sprague (1952) studied this question.
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