Abstract:
:Heparin-induced thrombocytopenia (HIT) is mediated by a heparin-dependent antibody/platelet factor 4/heparin complex binding to platelets via the Fc gamma receptor (type IIA). A single base polymorphism at position 131 of Fc gamma RIIA changes the native arginine to histidine. In the presence of murine monoclonal IgG1 the former phenotype (Fc gamma RIIAArg131) is functionally characterized by strong platelet aggregation (high responder) and the latter (Fc gamma RIIAHis131) by poor aggregation (low responder). In the presence of human IgG2 the opposite response is observed. It has recently been shown that the heparin-dependent antibody is predominantly of this subclass. We hypothesize that a relationship exists between Fc gamma RIIAHis131 and the development of HIT. We studied 24 normal individuals and 20 HIT patients using VM58, a murine monoclonal IgG1, to characterize the phenotype by platelet aggregrometry, and PCR products, amplified with primers bordering the Fc gamma RIIA polymorphism and hybridized with oligonucleotide probes specific for the single base mutation, to determine the genotype. The distribution of phenotypes and genotypes in the two populations differed, with a greater prevalence of the Fc gamma RIIAHis131 allele in the HIT patient population. Homozygous Fc gamma RIIAArg131 individuals were absent from this group. We conclude that the presence of the Fc gamma RIIAHis131 allele is associated with a predisposition to HIT.
journal_name
Br J Haematoljournal_title
British journal of haematologyauthors
Burgess JK,Lindeman R,Chesterman CN,Chong BHdoi
10.1111/j.1365-2141.1995.tb05383.xsubject
Has Abstractpub_date
1995-11-01 00:00:00pages
761-6issue
3eissn
0007-1048issn
1365-2141journal_volume
91pub_type
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