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W Lerner, R Caruso, D Faig and S Karpatkin
The mechanism of drug-dependent immunologic thrombocytopenic purpura (DITP)
was investigated by studying the sera of four patients with classic DITP
(two with quinidine-, one with acetaminophen-, and one with
phenazopyridine-dependent antiplatelet antibody) using a solid- phase
radioimmunoassay with 125I-staphylococcal protein A. Two forms of
antiplatelet antibody could be demonstrated: one that required drug to bind
to platelets and one that bound to platelets in the absence of drug.
Drug-dependent antiplatelet antibody required the simultaneous addition of
drug and the Fc domain of the drug-dependent IgG molecule for binding to
platelets. It did not require serum complement or factor VIII-related
antigen for binding to platelets. Drug-dependent binding of antibody to
platelets was saturation-dependent. Non-drug-dependent antiplatelet
antibody of two patients (one with quinidine-induced thrombocytopenia and
the other with acetaminophen-induced thrombocytopenia) reacted with
autologous platelets as well as with homologous platelets, indicating that
they were autoantibodies. Both autoantibodies had disappeared when their
sera were tested 23 and 138 days, respectively, after withdrawal of their
initial positive sera. Non-drug-dependent antiplatelet antibody binding
could be demonstrated with the F(ab')2 fragment of the purified IgG of the
serum of the second patient with quinidine DITP, who did not have
detectable alloantibodies against HLA. None of the four patients with
non-drug- dependent antiplatelet antibody had a past or present history of
autoimmune thrombocytopenic purpura.
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| Copyright © 1985 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
