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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 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 Citation Map 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. Related Collections Hemostasis, Thrombosis, and Vascular Biology Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report 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, Chloé Charroing, and Hervé Watier From the Department of Hematology-Hemostasis, Centre Hospitalier Universitaire (CHU) Tours, Institut National de la Santé et de la Recherche Médicale (INSERM) U618, Tours, France; the Unité Propre de Recherche de l'Enseignement Supérieur-Equipe d'Acceuil (UPRES-EA) "Immuno-Pharmaco-Genetics of therapeutic Antibodies", University of Tours, Tours, France; and the Laboratory of Hematology, Hôpital Necker and INSERM U428, Faculté de Pharmacie, Paris, France. We hypothesized that Fc receptor IIIa (FcRIIIa), a polymorphic receptor for the Fc portion of immunoglobulin G (IgG) other than FcRIIa, was involved 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 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 FcRIIa-131H/R polymorphism. In contrast, FcRIIIa-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 FcRIIIa-158V allotype, thus contributing to the development of thrombocytopenia. (Blood. 2004;104:2791-2793) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: 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] E. de Maistre, Y. Gruel, and D. Lasne Diagnosis and management of heparin-induced thrombocytopenia: [Le diagnostic et le traitement de la thrombopenie induite par l'heparine]. Can J Anesth, June 1, 2006; 53(6_suppl): S123 - S134. [Abstract] [Full Text] [PDF]

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