The platelet α2-integrin (GPIa) nucleotide-807 polymorphism is not associated with a risk for maternal–fetal human platelet antigen-5 incompatibility

Abstract

Alloimmunization against human platelet antigen (HPA)-5 may lead to neonatal alloimmune thrombocytopenia. The HPA-5 dimorphism is expressed on the platelet α2β1 integrin. The density of this receptor is associated with another dimorphism of the α2β1 integrin (nucleotide-807C/T). We hypothesized that anti-HPA-5b-induced neonatal thrombocytopenia is more likely to occur if the receptor is expressed at high than at low levels. Among 933 mother–child pairs, we identified 79 HPA-5aa mothers giving birth to a HPA-5ab offspring. Seventeen mothers had HPA-5b antibodies, but the offspring had a normal platelet count. We genotyped the offspring and mothers for the α2-807C/T dimorphism to evaluate its relationship to antibody formation. There was no difference between the frequency of the 807C/T dimorphism among children delivered from alloimmunized mothers and those from mothers without antibodies (P>0.3). The frequency of the 807C/T dimorphism was not different in the two maternal groups. In three maternal–fetal incompatibilities, we observed at delivery normal platelet counts of platelets typed HPA-5b-α2807T, despite increasing maternal antibody titers during the pregnancy. Our data do not support the hypothesis that the 807C/T dimorphism in the HPA-5ab children is a predisposing factor to either elicit alloimmunization against HPA-5b or for neonatal alloimmune thrombocytopenia.