血小板功能与动脉粥样硬化的研究进展

由于多种遗传因素和环境因素的影响,动脉粥样硬化的发病机制与血栓形成、脂质浸润及损伤炎症反应等有关.研究证实,血小板参与了动脉粥样硬化的形成过程,但其机制十分复杂,可能与血小板对内膜的损伤,释放出的细胞因子,以及相关脂蛋白的调节相关.     

Maternal platelet size as a marker for fetal trisomies 18 and 13

Maternal and fetal platelet size and glycoprotein expression were measured in 14 pregnancies complicated by fetal aneuploidy between 20 and 24 weeks' gestation. Flow cytometry was used to determine platelet size and surface glycoprotein Ib (GPIb) and GPIIIa expression both before and after stimulation with adenosine diphosphate (ADP). The data were compared with results obtained from 35 normal paired maternal and fetal controls. In fetuses affected with trisomies 18 and 13, but not trisomy 21, the maternal and fetal platelet sizes were significantly higher than those of the normal controls. Furthermore, the increase in fetal platelet size was significantly associated with the increase in maternal platelet size. Increase in maternal platelet size may be of potential value as a marker for fetal trisomies 18 and 13.     

Neonatal alloimmune thrombocytopenia due to anti-P1A1 (anti-hpa-1a): Importance of paternal and fetal platelet typing for assessment of fetal risk

Neonatal alloimmune thrombocytopenia (NAIT), which usually involves sensitization to P1^A1 (HPA-1a), may have devastating complications for the fetus. These may be prevented by antenatal treatment of severe cases with either maternally administered high-dose gamma-globulin and/or repeated intrauterine platelet transfusions. Determination of the paternal platelet phenotype is useful for counselling parents who have had one or more affected pregnancies. This report of an unaffected pregnancy in a woman with a history of previous pregnancies complicated by NAIT illustrates the role of paternal and fetal platelet phenotyping in managing existing pregnancies at risk of NAIT.