Posttransfusion purpura: conversion of PLA1-negative platelets to the PLA1-positive phenotype by stored plasma is not due to the presence of soluble PLA1 antigen.
Three previous articles have reported a PLA1 antigen in the plasma of stored blood which is capable of binding to PLA1-negative platelets in the presence of divalent cations, rendering them PLA1 positive. Such a mechanism could explain the enigma of posttransfusion purpura (PTP), i.e., severe thrombocytopenia in a healthy subject with PLA1-negative platelets secondary to the infusion of blood containing PLA1-positive platelets. We find that the PLA1 antigen of stored blood is due to the presence of platelet fragments which can be removed by centrifugation and that divalent cation-chelating agents play no role in the apparent binding of these fragments to platelets. The apparent conversion of PLA1-negative platelets to the PLA1-positive phenotype by incubation with stored plasma from a PLA1-positive subject is due to the cosedimentation of platelet fragments with the platelets. No soluble PLA1 antigen was found in the plasma of five patients with acute posttransfusion purpura.
Department of Medicine, New York University Medical School, New York 10016.
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Ehmann
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Dancis
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Ferziger
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Karpatkin
D016824:Antigens, Human Platelet; D001792:Blood Platelets / Q000276:immunology*; D000939:Epitopes; D006801:Humans; D039661:Integrin beta3; D007519:Isoantigens / Q000032:analysis*; D010641:Phenotype; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D011696:Purpura, Thrombocytopenic / Q000097:blood / Q000209:etiology*; D065227:Transfusion Reaction
D016824:Antigens, Human Platelet; D000939:Epitopes; C061248:ITGB3 protein, human; D039661:Integrin beta3; D007519:Isoantigens; D010980:Platelet Membrane Glycoproteins