Powers R W, Evans R W, Ness R B, Crombleholme W R, Roberts J M
Magee-Womens Research Institute Department of Ob/Gyn & Reproductive Sciences, Pittsburgh, Pennsylvania, USA.
Hypertens Pregnancy. 2001;20(1):69-77. doi: 10.1081/PRG-100104173.
The objective of this study was to confirm that endothelial dysfunction is present in preeclampsia and absent in transient hypertension of pregnancy, and to determine whether the cardiovascular risk factor homocysteine is associated with the degree of endothelial dysfunction.
We measured cellular fibronectin (as a marker of endothelial injury) and total plasma homocysteine in samples collected at the time of admittance to labor and delivery in 17 women with preeclampsia (increased blood pressure, proteinuria, and hyperuricemia), 16 women with transient hypertension of pregnancy (only increased blood pressure), and 34 normal pregnant women. Each subject with preeclampsia was matched by prepregnancy body mass index, race, and gestational age at delivery to one subject with transient hypertension of pregnancy and two controls.
Cellular fibronectin was found to be significantly increased in women with preeclampsia compared to subjects with transient hypertension of pregnancy or normal pregnant women (22.9 +/- 14.1 microg/mL versus 10.9 +/- 5.4 and 10.1 +/- 6.2 microg/mL, respectively, p<0.0001). Similarly, total plasma homocysteine was also significantly increased in the women with preeclampsia compared to subjects with transient hypertension of pregnancy or normal pregnant women (8.3 +/- 2.5 microM versus <5.5 +/- 2.2 and 5.4 +/- 3.4 microM respectively, p<0.01). However, contrary to our hypothesis, there was no apparent association between cellular fibronectin and homocysteine.
The increased concentrations of homocysteine observed in preeclampsia are not a general feature of all hypertensive complications of pregnancy. Furthermore, endothelial dysfunction is present in preeclampsia and is not evident in transient hypertension of pregnancy. However, the apparent endothelial dysfunction in preeclampsia is not explained by the increase in homocysteine concentrations observed.
本研究的目的是证实子痫前期存在内皮功能障碍,而妊娠短暂性高血压不存在内皮功能障碍,并确定心血管危险因素同型半胱氨酸是否与内皮功能障碍程度相关。
我们在17名单纯收缩期高血压(血压升高、蛋白尿和高尿酸血症)、16名妊娠短暂性高血压(仅血压升高)和34名正常孕妇分娩入院时采集的样本中测量细胞纤连蛋白(作为内皮损伤的标志物)和血浆总同型半胱氨酸。子痫前期的每一位受试者均按孕前体重指数、种族和分娩时的孕周与一名妊娠短暂性高血压受试者和两名对照进行匹配。
与妊娠短暂性高血压受试者或正常孕妇相比,子痫前期患者的细胞纤连蛋白显著增加(分别为22.9±14.1μg/mL、10.9±5.4μg/mL和10.1±6.2μg/mL,p<0.0001)。同样,与妊娠短暂性高血压受试者或正常孕妇相比,子痫前期患者的血浆总同型半胱氨酸也显著增加(分别为8.3±2.5μM、<5.5±2.2μM和5.4±3.4μM,p<0.01)。然而,与我们的假设相反,细胞纤连蛋白和同型半胱氨酸之间没有明显关联。
子痫前期观察到的同型半胱氨酸浓度升高并非妊娠所有高血压并发症的普遍特征。此外,子痫前期存在内皮功能障碍,而妊娠短暂性高血压中不明显。然而,子痫前期明显的内皮功能障碍不能用观察到的同型半胱氨酸浓度升高来解释。