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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2791-2793. Prepublished online as a Blood First Edition Paper on June 10, 2004; DOI 10.1182/blood-2004-01-0058. This Article Full Text (PDF) All Versions of this Article: 2004-01-0058v1 104/9/2791    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gruel, Y. Articles by Watier, H. Search for Related Content PubMed PubMed Citation Articles by Gruel, Y. Articles by Watier, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 8, 2004 Accepted April 13, 2004 The homozygous FcRIIIa-158V genotype is a risk factor for heparin-induced thrombocytopenia in patients with antibodies to heparin/platelet factor 4 complexes Yves Gruel*, Claire Pouplard, Dominique Lasne, Charlotte Magdelaine-Beuzelin, Chloe Charroing, and Herve Watier Hematology-Hemostasis and INSERM U618, University of Tours and IFR120, Tours, France Hematology-Hospital Necker and INSERM U428, Faculty of Pharmacy, Paris, France Immuno-Pharmaco-Genetics of Therapeutic Antibodies, University of Tours and IFR120, Tours, France * Corresponding author; email: gruel{at}med.univ-tours.fr. The involvement of FcRIIIa, a polymorphic receptor for the Fc portion of IgG other than FcRIIa, was hypothesized in heparin-induced thrombocytopenia (HIT). FcRIIa-131 and FcRIIIa-158 genotypes were determined in 102 patients with definite HIT and in 2 control groups of patients treated by heparin (86 subjects without detectable Abs to 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 FcRIIa-131H/R polymorphism. In contrast, FcRIIIa-158V homozygotes were more frequent in the HIT group than in the Ab+ group (p = 0.02), a difference which was more pronounced in patients with high levels of anti-H/PF4 Abs (p = 0.01). Since anti-H/PF4 Abs are mainly IgG1 and IgG3, clearance of sensitized platelets may be increased in patients homozygous for the FcRIIIa-158V allotype, thus contributing to the development of thrombocytopenia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Marin, R. Gonzalez-Conejero, P. Capranzano, T. A. Bass, V. Roldan, and D. J. Angiolillo Pharmacogenetics in cardiovascular antithrombotic therapy. J. Am. Coll. Cardiol., September 15, 2009; 54(12): 1041 - 1057. [Abstract] [Full Text] [PDF] T. E. Warkentin, J.-A. I. Sheppard, C. S. Sigouin, T. Kohlmann, P. Eichler, and A. Greinacher Gender imbalance and risk factor interactions in heparin-induced thrombocytopenia Blood, November 1, 2006; 108(9): 2937 - 2941. [Abstract] [Full Text] [PDF]

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