Kiefel V, Meyer E, Greinacher A, Kroll H, Mueller-Eckhardt C
Institut für klinische Immunologie und Transfusionsmedizin, Justus-Liebig-Universität Giessen, BRD.
Beitr Infusionsther. 1992;30:450-3.
Neonatal alloimmune thrombocytopenic purpura is caused by maternal platelet-specific alloantibodies which react on fetal platelets with the corresponding antigen. We describe a 30-year-old female patient with type I Glanzmann thrombasthenia who developed an isoantibody against the platelet GP IIb/IIIa complex before or during pregnancy. The platelet count in the male newborn was 35 x 10(9)/l, but there were no signs of cerebral hemorrhage. Following infusion of 2 g/day i.v. IgG on 3 consecutive days, platelet counts rose to normal values. An isoantibody reacting with the GP IIb/IIIa complex of all platelet donors tested was found in the maternal serum using the MAIPA assay. Thus, immune-mediated neonatal thrombocytopenia may be caused by platelet isoantibodies against GP IIb/IIIa as well as by platelet-specific alloantibodies and by maternal autoantibodies.
新生儿同种免疫性血小板减少性紫癜是由母体血小板特异性同种抗体引起的,这些抗体与胎儿血小板上相应的抗原发生反应。我们描述了一名30岁患有I型Glanzmann血小板无力症的女性患者,她在怀孕前或怀孕期间产生了针对血小板糖蛋白IIb/IIIa复合物的同种抗体。男婴的血小板计数为35×10⁹/L,但没有脑出血的迹象。连续3天每天静脉注射2g免疫球蛋白后,血小板计数升至正常水平。使用单克隆抗体固相血小板抗原捕获试验(MAIPA)在母体血清中发现了一种与所有检测的血小板供体的糖蛋白IIb/IIIa复合物发生反应的同种抗体。因此,免疫介导的新生儿血小板减少症可能由针对糖蛋白IIb/IIIa的血小板同种抗体、血小板特异性同种抗体以及母体自身抗体引起。