作者: Yves Gruel , Claire Pouplard , Dominique Lasne , Charlotte Magdelaine-Beuzelin , Chloé Charroing
DOI: 10.1182/BLOOD-2004-01-0058
关键词: Immunoglobulin G 、 Platelet 、 Allotype 、 Platelet factor 4 、 Heparin-induced thrombocytopenia 、 Genotype 、 Heparin 、 Antibody 、 Medicine 、 Immunology 、 Cell biology 、 Biochemistry 、 Hematology
摘要: We hypothesized that Fcγ receptor IIIa (FcγRIIIa), a polymorphic for the Fc portion of immunoglobulin G (IgG) other than FcγRIIa, was involved in heparin-induced thrombocytopenia (HIT). FcγRIIa-131 and FcγRIIIa-158 genotypes were determined 102 patients with definite HIT 2 control groups treated by heparin (86 subjects without detectable antibodies [Abs] to heparin-platelet factor 4 [H/PF4], Ab - group; 84 Abs H/PF4 HIT, + group). There no significant differences genotype distribution or allele frequencies between 3 FcγRIIa-131H/R polymorphism. In contrast, FcγRIIIa-158V homozygotes more frequent group ( P = .02), difference pronounced high levels anti-H/PF4 .01). Since are mainly IgG1 IgG3, clearance sensitized platelets may be increased homozygous allotype, thus contributing development thrombocytopenia. (Blood. 2004;104:2791-2793)