Prenatal Platelet Genotyping for Neonatal Alloimmune Thrombocytopenia.

为了揭示母体对血小板抗原（HPA）的同种免疫的流行率和新生儿同种免疫性血小板减少症（NAT）的发生率，使用混合被动血凝试验检测了10，000份母体血清中抗HPA抗体的存在。抗HPA抗体阳性96例，抗HPA-4b抗体阳性23例，抗HPA-5a抗体阳性2例，抗HPA-5b抗体阳性70例，抗Nak ^a抗体阳性1例。我们探讨了应用序列特异性引物-聚合酶链反应（PCR-SSP）扩增羊膜细胞DNA进行胎儿HPA-4基因分型的可行性。3例羊水细胞中胎儿HPA-4型与自身血中HPA-4型完全一致。两个胎儿显示为纯合子PHA-4a/a，血小板计数正常。第三胎为杂合子HPA-4a/B，与母体抗体不相容，并出现血小板减少症。结果表明，DNA扩增法可用于羊水中HPA-4基因分型。

To reveal the prevalence of maternal alloimmunization to platelet antigens (HPA) and the incidence of neonatal alloimmune thrombocytopenia (NAT), 10,000 maternal sera were tested for the presence of anti-HPA antibodies using the Mixed Passive Haemagglutination. Ninety-six anti-HPA were found ; anti-HPA-4b, -5a, -5b and anti-Nak^a in 23,2,70 and one pregnant women, respectively.Optimal management of NAT requires the determination of fetal HPA status as early as possible. We explored the feasibility of fetal HPA-4 genotyping by amplification of DNA from amniotic cells using sequence specific primers-polymerase chain reaction (PCR-SSP). Three babies in which fetal HPA-4 type from amniotic fluid cells was completely concordant with type using the blood of these infants studied. Two fetuses were shown to be homozygous PHA-4a/a, and had normal platelet counts. The third fetus was heterozygous HPA-4a/b incompatible with maternal antibody, and developed thrombocytopenia. These findings suggest that HPA-4 genotyping can be reliable determinied from amniotic fluid by DNA amplification.