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子痫前期的病理生理学及母体生物学标志物

Pathophysiology and maternal biologic markers of preeclampsia.

作者信息

Massé Jacques, Giguère Yves, Kharfi Abdelaziz, Girouard Joël, Forest Jean-Claude

机构信息

Perinatology Research Unit, Hôpital Saint-François d'Assise Research Center, CHUQ, Quebec City, Quebec, Canada.

出版信息

Endocrine. 2002 Oct;19(1):113-25. doi: 10.1385/ENDO:19:1:113.

DOI:10.1385/ENDO:19:1:113
PMID:12583608
Abstract

Preeclampsia-increased blood pressure and proteinuria appearing after the twentieth week of pregnancy--is a major cause of materal and neonatal morbidity, leading to iatrogenic prematurity. Several lines of evidence suggest that the disorder is owing to diminished invasion of spiral arteries by trophoblastic cells, followed by reduced perfusion of the fetoplacental unit and oxidative stress. These alterations, in the presence of maternal predisposition, lead to endothelial dysfunction and occurrence of the clinical syndrome of preeclampsia (multisystemic lesions). Although the pathophysiology of preeclampsia is still unknown, progress has been made during the past 10 yr, and the early identification of at-risk women with the use of biochemical; ultrasonographic; and, more recently, genetic susceptibility markers has been the subject of intense research. In the present review, markers of maternal predisposition, placental implantation, oxidative stress, vasomotor regulation, and endothelial dysfunction are investigated as candidate markers in the early prediction of preeclampsia. Unfortunately, at the present time, no marker has been proven to have a clinically useful predictive performance in the general pregnant population, and, therefore, more research in that area is warranted.

摘要

子痫前期——妊娠20周后出现的血压升高和蛋白尿——是孕产妇和新生儿发病的主要原因,可导致医源性早产。多项证据表明,该病症是由于滋养层细胞对螺旋动脉的侵入减少,继而导致胎儿 - 胎盘单位灌注减少和氧化应激所致。在存在母体易感性的情况下,这些改变会导致内皮功能障碍和子痫前期临床综合征(多系统病变)的发生。尽管子痫前期的病理生理学仍不清楚,但在过去10年中已取得进展,利用生化、超声检查以及最近的遗传易感性标记物对高危女性进行早期识别一直是深入研究的主题。在本综述中,对母体易感性、胎盘植入、氧化应激、血管舒缩调节和内皮功能障碍的标记物作为子痫前期早期预测的候选标记物进行了研究。不幸的是,目前尚无标记物被证明在一般孕妇群体中具有临床有用的预测性能,因此,该领域需要更多的研究。

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Pathophysiology and maternal biologic markers of preeclampsia.子痫前期的病理生理学及母体生物学标志物
Endocrine. 2002 Oct;19(1):113-25. doi: 10.1385/ENDO:19:1:113.
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Current concepts in preeclampsia.
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[Endothelial dysfunction: role in the maternal syndrome of preeclampsia and long-term consequences for the cardiovascular system].[内皮功能障碍:在子痫前期母体综合征中的作用及对心血管系统的长期影响]
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Role of oxidative stress in the pathogenesis of preeclampsia.氧化应激在子痫前期发病机制中的作用。
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[Pathophysiology and clinical manifestations in pre-eclampsia].[子痫前期的病理生理学与临床表现]
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Endocrine. 2013 Apr;43(2):387-93. doi: 10.1007/s12020-012-9766-0. Epub 2012 Aug 17.

本文引用的文献

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Studies on autonomic blockade. VI. The mechanisms regulating the hemodynamic changes in the pregnant woman and their relation to the hypertension of toxemia of pregnancy.
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Early pregnancy levels of pregnancy-associated plasma protein a and the risk of intrauterine growth restriction, premature birth, preeclampsia, and stillbirth.妊娠相关血浆蛋白A的早期妊娠水平与胎儿宫内生长受限、早产、子痫前期和死产风险
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Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia.母体和胎儿遗传性血栓形成倾向与重度子痫前期的发生无关。
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Apolipoprotein E alleles in women with pre-eclampsia.先兆子痫女性中的载脂蛋白E等位基因
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Angiotensinogen and endothelial nitric oxide synthase gene polymorphisms among Hispanic patients with preeclampsia.子痫前期西班牙裔患者血管紧张素原和内皮型一氧化氮合酶基因多态性
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