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Maternal PE frequently occurs with FGR and shares many similar pathologic features.^{91, 92} PE is part of the spectrum of hypertensive disorders in pregnancy and is typically defined by new‐onset maternal hypertension plus proteinuria after 20 weeks of gestation. As proteinuria measurements can be unreliable,⁹³ maternal hypertension in conjunction with other features, including FGR, may alternatively be used for diagnosis.⁹⁴ Early‐onset PE (EOPE), defined as onset <34 weeks of gestational age, is generally more severe and more commonly associated with FGR than late‐onset PE (LOPE).⁹⁵ These appear to be distinct entities with placental pathology playing a greater role in EOPE.⁹⁶ Gene expression changes have also been used to demonstrate heterogeneity among PE‐associated placentas, with only a subset showing alterations in classical markers of angiogenesis, such as sFLT‐1 and sENG.^97–100

Preeclamptic placentas exhibit areas of syncytial knots (clusters of pre‐apoptotic/apoptotic nuclei) and areas of necrosis associated with loss of the syncytial trophoblast microvillous membranes (STMBs).¹⁰¹ These STMB fragments are released into the mother's blood and have disrupting effects on the maternal endothelium.¹⁰² Correspondingly, increased maternal serum levels of cell‐free fetal (i.e. placental) DNA have been reported in PE; however, this may not be predictive after accounting for associated maternal characteristics.¹⁰³ Furthermore, measuring the ratio of fetal/placental to maternal cell‐free DNA may have limited predictive power for PE as the maternal cell‐free DNA may also increase in these pregnancies.¹⁰⁴