Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The University of Chicago, Chicago, IL.
Department of Medicine, Obstetrics, and Gynecology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Am J Obstet Gynecol. 2022 Feb;226(2S):S1019-S1034. doi: 10.1016/j.ajog.2020.10.022. Epub 2020 Oct 20.
Preeclampsia is a devastating medical complication of pregnancy that can lead to significant maternal and fetal morbidity and mortality. It is currently believed that there is abnormal placentation in as early as the first trimester in women destined to develop preeclampsia. Although the etiology of the abnormal placentation is being debated, numerous epidemiologic and experimental studies suggest that imbalances in circulating angiogenic factors released from the placenta are responsible for the maternal signs and symptoms of preeclampsia. In particular, circulating levels of soluble fms-like tyrosine kinase 1, an antiangiogenic factor, are markedly increased in women with preeclampsia, whereas free levels of its ligand, placental, growth factor are markedly diminished. Alterations in these angiogenic factors precede the onset of clinical signs of preeclampsia and correlate with disease severity. Recently, the availability of automated assays for the measurement of angiogenic biomarkers in the plasma, serum, and urine has helped investigators worldwide to demonstrate a key role for these factors in the clinical diagnosis and prediction of preeclampsia. Numerous studies have reported that circulating angiogenic biomarkers have a very high negative predictive value to rule out clinical disease among women with suspected preeclampsia. These blood-based biomarkers have provided a valuable tool to clinicians to accelerate the time to clinical diagnosis and minimize maternal adverse outcomes in women with preeclampsia. Angiogenic biomarkers have also been useful to elucidate the pathogenesis of related disorders of abnormal placentation such as intrauterine growth restriction, intrauterine fetal death, twin-to-twin transfusion syndrome, and fetal hydrops. In summary, the discovery and characterization of angiogenic proteins of placental origin have provided clinicians a noninvasive blood-based tool to monitor placental function and health and for early detection of disorders of placentation. Uncovering the mechanisms of altered angiogenic factors in preeclampsia and related disorders of placentation may provide insights into novel preventive and therapeutic options.
子痫前期是一种严重的妊娠并发症,可导致母婴发病率和死亡率显著增加。目前认为,在注定会发展为子痫前期的女性中,早在妊娠早期就存在胎盘异常。虽然胎盘异常的病因仍存在争议,但大量的流行病学和实验研究表明,胎盘释放的循环血管生成因子失衡是导致子痫前期母体症状的原因。特别是,子痫前期妇女的可溶性 fms 样酪氨酸激酶 1(一种抗血管生成因子)循环水平显著升高,而其配体胎盘生长因子的游离水平则显著降低。这些血管生成因子的改变先于子痫前期临床症状的出现,并与疾病的严重程度相关。最近,用于测量血浆、血清和尿液中血管生成生物标志物的自动化检测方法的出现,帮助世界各地的研究人员证明了这些因子在子痫前期的临床诊断和预测中的关键作用。大量研究报告称,循环血管生成生物标志物对排除疑似子痫前期妇女的临床疾病具有非常高的阴性预测值。这些基于血液的生物标志物为临床医生提供了一个有价值的工具,可以加速临床诊断的时间,并最大限度地减少子痫前期妇女的不良母婴结局。血管生成生物标志物也有助于阐明与胎盘异常相关的疾病的发病机制,如宫内生长受限、胎儿宫内死亡、双胎输血综合征和胎儿水肿。总之,胎盘源性血管生成蛋白的发现和特征为临床医生提供了一种非侵入性的基于血液的工具,用于监测胎盘功能和健康,并早期发现胎盘异常。揭示子痫前期和相关胎盘异常中改变的血管生成因子的机制可能为新的预防和治疗方法提供思路。