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Increased expression of platelet IgG Fc receptors in immune heparin-
induced thrombocytopenia
BH Chong, RL Pilgrim, MA Cooley and CN Chesterman
Department of Haematology, Prince of Wales Hospital, University of New
South Wales, Sydney, Australia.
Our previous finding that heparin-dependent antibodies in heparin- induced
thrombocytopenia (HIT) bind to platelets via platelet IgG Fc receptors
(FcRs) prompted this study. Platelet FcRs in 16 patients with HIT, 23
control patients, and 42 normal subjects were studied. Patients with HIT
had substantially increased platelet FcRs during the acute illness. Those
who suffered serious thrombotic complications or died shortly after
diagnosis had significantly more FcRs per platelet than those with milder
disease. Consistent with their increased FcRs, platelets of patients with
HIT showed increased aggregation reactivity to aggregated IgG and
heparin-dependent antibodies. Platelet FcRs in patients with HIT remained
elevated for 1 to 3 months after the acute illness then stabilized to a
mean value not significantly different from either control group. The
increased expression of FcRs on HIT platelets and their increased
reactivity to heparin-dependent antibodies may contribute to the
pathogenesis of thrombocytopenia and thrombosis in HIT.
Volume 81,
Issue 4,
pp. 988-993,
02/15/1993
Copyright © 1993 by The American Society of Hematology
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