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Introduction The suggestion that antibodies to platelets are responsible for the thrombocytopenia of "idiopathic" thrombocytopenic purpura (ITP) is based on three observations: (a) infants born of mothers with ITP sometimes exhibit thrombocytopenia¹; (b) normal volunteers who receive infusions of plasma from patients with ITP sometimes develop thrombocytopenia²; (c) transfused platelets do not circulate as long in patients with ITP as in normal recipients.³These phenomena indicate that a constituent of the blood of some patients with ITP is able to depress platelet levels of normal persons. These observations, however, are not proof of an antigen-antibody reaction, and it is not known whether this platelet-depressing activity is, in fact, capable of affecting the patient's own platelets. Platelet antibodies have been demonstrated in patients with thrombocytopenia induced by drugs, such as allyl-isopropyl-acetyl-carbamide (Sedormid),⁴quinidine,⁵quinine,⁶and novobiocin⁷; and in patients who have received transfusions.⁸⁻¹⁰
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Milton Corn (1962) studied this question.
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