Aardema M W, Saro M C S, Lander M, De Wolf B T H M, Oosterhof H, Aarnoudse J G
Department of Obstetrics and Gynaecology, Division of Obstetrics and Perinatal Medicine, University Medical Centre Groningen, Postbox 30.001, 9700 RB Groningen, The Netherlands.
Clin Sci (Lond). 2004 Apr;106(4):377-82. doi: 10.1042/CS20030385.
The 'classical' concept that pregnancy-induced hypertension (PIH) and pre-eclampsia (PE) primarily originate from defective placentation in early pregnancy has been challenged recently. There is growing evidence that other factors, including maternal predisposing conditions, also play a significant role in the pathophysiology of PIH and PE. The aim of the present study was to test the hypothesis that PIH and PE with an early onset and poor pregnancy outcome is associated with defective placentation, e.g. inadequate spiral artery dilatation and subsequent reduced uteroplacental perfusion, whereas PIH and PE with normal pregnancy outcome is not. Using Doppler ultrasound, we measured the uterine artery pulsatility index (PI) in a population of 531 nulliparous women in the 22nd week of gestation. Uterine artery PI was used as an index of resistance to blood flow in the uteroplacental circulation. Outcome measures were PIH/PE with or without poor pregnancy outcome, preterm birth and intra-uterine growth restriction (IUGR). The results revealed a striking difference between PI values for PIH/PE with and without poor pregnancy outcome. Uterine artery PI in the 22nd week was increased significantly in pregnancies which developed early-onset (before 35 weeks) PIH/PE with a poor pregnancy outcome. In contrast, uterine artery PI values were normal in women who developed PIH/PE, but had a good pregnancy outcome. There was a significant correlation between 22nd week uterine artery PI and subsequent preterm birth or IUGR. Our results indicate that only PIH/PE with poor pregnancy outcome is associated with defective placentation, whereas PIH/PE with good outcome is not. These findings support the concept of heterogeneous causes of hypertensive disorders of pregnancy.
妊娠高血压(PIH)和先兆子痫(PE)主要源于妊娠早期胎盘形成缺陷这一“经典”概念最近受到了挑战。越来越多的证据表明,包括母体易感因素在内的其他因素在PIH和PE的病理生理过程中也起着重要作用。本研究的目的是检验以下假设:早发型且妊娠结局不良的PIH和PE与胎盘形成缺陷有关,例如螺旋动脉扩张不足及随后子宫胎盘灌注减少,而妊娠结局正常的PIH和PE则不然。我们使用多普勒超声对531名妊娠22周的未生育女性测量了子宫动脉搏动指数(PI)。子宫动脉PI被用作子宫胎盘循环中血流阻力的指标。观察指标为有无不良妊娠结局的PIH/PE、早产和宫内生长受限(IUGR)。结果显示,有无不良妊娠结局的PIH/PE的PI值存在显著差异。在发生早发型(35周前)且妊娠结局不良的PIH/PE的妊娠中,第22周时子宫动脉PI显著升高。相比之下,发生PIH/PE但妊娠结局良好的女性子宫动脉PI值正常。第22周子宫动脉PI与随后的早产或IUGR之间存在显著相关性。我们的结果表明,只有妊娠结局不良的PIH/PE与胎盘形成缺陷有关,而妊娠结局良好的PIH/PE则不然。这些发现支持了妊娠高血压疾病病因异质性的概念。