Placental angiogenic growth factors and uterine artery Doppler findings for characterization of different subsets in preeclampsia and in isolated intrauterine growth restriction
Placental angiogenic growth factors and uterine artery Doppler findings for characterization of different subsets in preeclampsia and in isolated intrauterine growth restriction
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DOI：
10.1016/j.ajog.2006.01.014
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发表时间：
2006-07-01
影响因子：
9.8
通讯作者：
Gratacos, Eduard
中科院分区：
文献类型：
--
作者：
Crispi, Fatima;Dominguez, Carmen;Gratacos, Eduard
目的：本研究的目的是评估胎盘标志物与子痫前期内皮功能障碍和宫内生长受限之间的可能关系。研究设计：前瞻性研究纳入早发型（< 34孕周）和晚发型的76例先兆子痫患者和37例宫内生长受限患者，以及40例对照组。测定血浆胎盘生长因子、可溶性膜样酪氨酸激酶i、血管细胞黏附分子i水平及子宫动脉多普勒指数。结果：早发性子痫前期和宫内生长受限组胎盘生长因子低于对照组，可溶性膜样酪氨酸激酶- i和血管细胞粘附分子- i高于对照组，但这些变化在子痫前期更为明显。在迟发性子痫前期，子宫动脉多普勒指数异常的患者可溶性类膜样酪氨酸激酶- i和血管细胞粘附分子- i水平较高。结论：早发性子痫前期及宫内生长受限的生化变化提示胎盘常见紊乱及内皮功能障碍状态，可能需要与其他因素相互作用才能解释子痫前期母体疾病。迟发性先兆子痫的数据表明，其中一部分可能发生在最小的胎盘受累情况下。(c) 2006 Mosby, Inc。版权所有。
Objective: The purpose of this study was to evaluate possible relationships between placental markers and endothelial dysfunction in preeclampsia and intrauterine growth restriction.Study design: A prospective study was conducted in 76 patients with preeclampsia and 37 patients with intrauterine growth restriction that were classified as early onset (< 34 weeks of gestational age) or late onset, and 40 control subjects. Plasma levels of placental growth factor, soluble fms-like tyrosine kinase-I, vascular cell adhesion molecule-I, and uterine artery Doppler indices were measured.Results: In early-onset preeclampsia and intrauterine growth restriction, placental growth factor was lower and soluble fms-like tyrosine kinase-I and vascular cell adhesion molecule-I higher than in control subjects, although all changes were more pronounced in preeclampsia. In late-onset preeclampsia, those patients with abnormal uterine artery Doppler indices had higher soluble fms-like tyrosine kinase-I and vascular cell adhesion molecule-I levels.Conclusion: Biochemical changes in early-onset preeclampsia and intrauterine growth restriction point to a common placental disorder and a state of endothelial dysfunction, which may require interaction with other factors to explain the maternal disease in preeclampsia. Data in late-onset preeclampsia suggest that a proportion of them may occur with minimal placental involvement. (c) 2006 Mosby, Inc. All rights reserved.