Baker P N, Krasnow J, Roberts J M, Yeo K T
Magee-Womens Research Institute, University of Pittsburgh, School of Medicine, Pennsylvania, USA.
Obstet Gynecol. 1995 Nov;86(5):815-21. doi: 10.1016/0029-7844(95)00259-T.
To determine whether altered levels of vascular endothelial growth factor (VEGF) may be implicated in the pathogenesis of preeclampsia, and whether VEGF mediates the endothelial cell activation that is involved in the pathogenesis of the clinical syndrome.
In a cross-sectional study, maternal serum samples in late pregnancy (at the time of clinical disease) were collected from 78 nulliparous women. These subjects were subdivided into those with preeclampsia (n = 27), nonproteinuric pregnancy-induced hypertension (n = 15), and normal pregnant women (n = 36). In a nested case-control study, in addition to samples taken before delivery, samples were obtained in early pregnancy (before clinical disease) and 24-48 hours postpartum from 12 of the patients with preeclampsia, 12 of those with nonproteinuric pregnancy-induced hypertension, and 12 of the normal pregnant subjects. Umbilical cord blood was sampled from 14 of the preeclamptic and 16 of the normal pregnant subjects. We measured VEGF levels in all samples using an immunofluorometric assay.
In most samples collected before delivery, VEGF levels were below the lower limit of detection. However, the proportion of detectable levels was higher in the preeclampsia group (seven of 27) than in the normotensive group (one of 36, P < .05). The proportion in the nonproteinuric pregnancy-induced hypertension group (two of 15) did not differ significantly from the other groups. Levels in the patients with preeclampsia were not elevated before clinical disease. Levels of VEGF in umbilical blood samples were higher than in maternal venous blood, although there were no significant differences between groups.
Serum VEGF levels were elevated in patients with preeclampsia, which suggests that the growth factor has a role in the endothelial cell activation that occurs in the disease.
确定血管内皮生长因子(VEGF)水平的改变是否与子痫前期的发病机制有关,以及VEGF是否介导了参与该临床综合征发病机制的内皮细胞活化。
在一项横断面研究中,从78名未生育妇女中收集了妊娠晚期(临床疾病发生时)的母血样本。这些受试者被分为子痫前期患者(n = 27)、无蛋白尿性妊娠高血压患者(n = 15)和正常孕妇(n = 36)。在一项巢式病例对照研究中,除了分娩前采集的样本外,还从12名单纯性子痫前期患者、12名无蛋白尿性妊娠高血压患者和12名正常孕妇中在妊娠早期(临床疾病出现前)和产后24 - 48小时采集了样本。从14名单纯性子痫前期患者和16名正常孕妇中采集了脐带血。我们使用免疫荧光分析法测量了所有样本中的VEGF水平。
在大多数分娩前采集的样本中,VEGF水平低于检测下限。然而,子痫前期组中可检测水平的比例(27例中的7例)高于血压正常组(36例中的1例,P <.05)。无蛋白尿性妊娠高血压组(15例中的2例)的比例与其他组无显著差异。子痫前期患者在临床疾病出现前VEGF水平并未升高。脐带血样本中的VEGF水平高于母静脉血,尽管各组之间无显著差异。
子痫前期患者血清VEGF水平升高,这表明该生长因子在该疾病中发生的内皮细胞活化中起作用。