Abstract |
We hypothesized that Fcgamma receptor IIIa (FcgammaRIIIa), a polymorphic receptor for the Fc portion of immunoglobulin G ( IgG) other than FcgammaRIIa, was involved in heparin-induced thrombocytopenia (HIT). FcgammaRIIa-131 and FcgammaRIIIa-158 genotypes were determined in 102 patients with definite HIT and in 2 control groups of patients treated by heparin (86 subjects without detectable antibodies [Abs] to heparin- platelet factor 4 [H/PF4], Ab(-) group; 84 patients with Abs to H/PF4 without HIT, Ab(+) group). There were no significant differences in genotype distribution or allele frequencies between the 3 groups for FcgammaRIIa-131H/R polymorphism. In contrast, FcgammaRIIIa-158V homozygotes were more frequent in the HIT group than in the Ab(+) group (P = .02), a difference that was more pronounced in patients with high levels of anti-H/PF4 Abs (P = .01). Since anti-H/PF4 Abs are mainly IgG1 and IgG3, clearance of sensitized platelets may be increased in patients homozygous for the FcgammaRIIIa-158V allotype, thus contributing to the development of thrombocytopenia.
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Authors | Yves Gruel, Claire Pouplard, Dominique Lasne, Charlotte Magdelaine-Beuzelin, Chloé Charroing, Hervé Watier |
Journal | Blood
(Blood)
Vol. 104
Issue 9
Pg. 2791-3
(Nov 01 2004)
ISSN: 0006-4971 [Print] United States |
PMID | 15191947
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antigens, CD
- Autoantibodies
- FCGR3A protein, human
- Fc gamma receptor IIA
- Receptors, IgG
- Platelet Factor 4
- Heparin
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Topics |
- Antigens, CD
(genetics)
- Autoantibodies
(blood)
- Case-Control Studies
- Gene Frequency
- Heparin
(adverse effects, immunology)
- Homozygote
- Humans
- Platelet Factor 4
(immunology)
- Polymorphism, Single Nucleotide
(physiology)
- Receptors, IgG
(genetics)
- Risk Factors
- Thrombocytopenia
(chemically induced, genetics, immunology)
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