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Evaluation of Platelet Antibodies in Idiopathic Thrombocytopenic Purpura
MILTON CORN, M.D.;
JEFFERSON D. UPSHAW, JR., M.D.
Arch Intern Med. 1962;109(2):157-167.
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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.3 These 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),4 quinidine,5 quinine,6 and novobiocin7; and in patients who have received transfusions.8-10
. . . [Full Text PDF of this Article]
Author Affiliations
BALTIMORE
From the Department of Medicine of The Johns Hopkins University and Hospital.; Fellow in Medicine, American Heart Association (Dr. Corn); Fellow in Medicine, American Cancer Society (Dr. Upshaw).
Footnotes
Submitted for publication Dec. 30, 1960.
This work was carried out under Contract AT (30-1) 1208 between the Atomic Energy Commission and The Johns Hopkins University and was supported in part by a research grant from the Division of Grants of the National Institutes of Health, U.S. Public Health Service.
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