遗传性父本抗原诱发妊娠期血小板减少症

本研究动态观察和分析1例分娩后母亲体内携带的遗传性父本抗原(IPA)与妊娠期血小板减少症的关系。检测患者自妊娠至分娩后2年以及新生儿至1岁时的血小板数变化,常规检测患者幽门螺旋杆菌、CMV、EBV、微小病毒及其他疱疹病毒感染。IPA检测是从基因文库选择8个在中国人群中多态性强的插入/缺失(InDel)多态性位点,设计引物,用巢式PCR和实时定量PCR检测54对健康的母子对,获得平均值作为对照,利用母子间两个有InDel多态性的位点来确定母子之间微嵌合状态,分别检测患者4个时间段携带IPA情况。结果表明,患者从妊娠20周开始血小板减少,最低10×109/L,用丙种球蛋白可使血小板数短期恢复,停药后又迅速减少。未检测到病毒和幽门螺旋杆菌感染。54例母体内IPA平均值10-5—10-4,该患者产后67 d IPA为3.45×10-3(此时血小板数为14×109/L),明显高于正常值30倍以上,1个月后为1.3×10-4(血小板数256×109/L),5个月为1.2×10-4(血小板数158×109/L),6个月1.5×10-4(血小板数325×109/L),达到正常母体水平,血小板恢复正常。新生儿出生1个月血小板减少(4×109/L),经大剂量丙种球蛋白治疗后恢复。结论:母体存在异常高IPA可能导致妊娠血小板减少症的发生。

Inherited Paternal Antigens Induce Pregnancy Thrombocytopenia

Objective of this study was to investigate the correlation of body-carried inherited paternal antigens （IPA） in one mother after delivery with pregnancy thrombocytopenia. The changes of platelet （Pit） count in the mother who deliveried 2 years ago and her child who is now one year＇s old were detected, routine tests included He licobacter pylori, CMV, EBV, parvovirus and other herpes virus＇ s infection were carried out. Eight insertion or deletion sites （InDel） SNP with strong polymorphisms in Chinese population was selected to detect IPA from a genomic library, then primers were designed, the nested PCR and real-time quantitative PCR were used to detect 54 healthy mother-child pairs, the obtained average value was taken as the control, finally two InDel polymorphism sites between mother and child were used to identify the mother/child microchimerism. The IPA of the mother were examined at 4 time points. The results showed that the Plt level of the mother who had suffered thrombocytopenia since 20 weeks after pregnancy reduced to 10×10^9/L. After using gamma globulin, the Pit count increased gradually, but the Pit count decreased rapidly when withdrawal. This patient did not have the infections of virus and Helicobacter pylori. IPA average value of 54 cases were from 10^-5 to 10^-4. At 67 d after delivery, the Pit count of the mother was 14 ×10^9/L, IPA was 3.45 ×10^-3, which was 30 times higher than the normal. In one month after treatment the IPA was 1.3 ×10^-4 （ Pit 256 ×10^9/L） , 5 months later it was 1.2 ×10^-4（Plt 158 ×10^9/L）, and 6 months later it was 1.5×10^-4（Plt 325 ×10^9/L）. When IPA reached the normal level, the Pit count returned to normal. Her child suffered thrombocytopenia （4 ×10^9/L） one month after he was born, then recovered after high-dose gamma globulin therapy. It is concluded that abnormal high level IPA may lead to pregnancy thrombocytopenia.