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Blood, Vol. 92 No. 5 (September 1), 1998:
pp. 1526-1531
Heparin-Induced Thrombocytopenia: New Insights Into the Impact of
the Fc RIIa-R-H131 Polymorphism
Lena E. Carlsson,
Sentot Santoso,
Gudrun Baurichter,
Hartmut Kroll,
Stephanie Papenberg,
Petra Eichler,
Nomdo A.C. Westerdaal,
Volker Kiefel,
Jan G.J. van de Winkel, and
Andreas Greinacher
From the Department of Immunology and Transfusion Medicine,
Ernst-Moritz-Arndt-University, Greifswald, Germany; the Department of
Clinical Immunology and Transfusion Medicine, Justus-Liebig-University,
Giessen, Germany; the Department of Immunology and Medarex Europe,
University Hospital Utrecht, Utrecht, The Netherlands; and the
Department of Immunology and Transfusion Medicine, University of
Leipzig, Leipzig, Germany.
Heparin-induced thrombocytopenia (HIT), a severe complication of
heparin treatment, can be associated with new thrombotic complications.
HIT antibodies activate platelets via the platelet Fc -receptor
(FcRIIa), which carries a functionally relevant polymorphism
(FcRIIa-R-H131). The effect of this polymorphism on the clinical
manifestations of HIT is controversial. We determined prospectively the
FcRIIa-R-H131 genotypes in 389 HIT patients, in 351 patients with
thrombocytopenia or thrombosis due to causes other than HIT and without
detectable HIT antibodies, and in 256 healthy blood donors. For this
purpose, a novel nested sequence-specific primer-polymerase chain
reaction (SSP-PCR) was developed. FcRIIa-R/R131 was
found to be overrepresented in the HIT patients (27%) compared with
the control groups (non-HIT patients [21%] and blood donors [20%]). In a subgroup of 122 well-characterized HIT patients, the
genotype distribution in patients presenting with thrombocytopenia only
was compared with that of patients who developed thromboembolic complications. The frequency of FcRIIa-R/R131 among patients with
thrombotic events was significantly elevated (37% v 17%; P = .036). Our results indicate that genotype distribution
can be correlated to the clinical outcome of patients with HIT. We speculate that the reduced clearance of immune complexes in patients with the FcRIIa-R/R131 allotype causes prolonged activation of endothelial cells and platelets, thus increasing the risk for thrombotic complications.
© 1998 by The American Society of Hematology.
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