Clausen Peter, Ekbom Pia, Damm Peter, Feldt-Rasmussen Ulla, Nielsen Birthe, Mathiesen Elisabeth R, Feldt-Rasmussen Bo
Department of Nephrology and Endocrinology, Copenhagen University Hospital, Rigshospitalet, DK-2100, Copenhagen, Denmark.
J Diabetes Complications. 2007 Sep-Oct;21(5):288-93. doi: 10.1016/j.jdiacomp.2006.03.004.
This study aims to test the hypothesis that vascular dysfunction is present early in pregnancy in women with type 1 diabetes who subsequently develop preeclampsia.
Eighty-three women with type 1 diabetes of more than 10 years duration were followed up prospectively during pregnancy. External ultrasound was used to measure the dilatory response of the brachial artery to postischemic increased blood flow (endothelium-dependent, flow-associated dilatation) and to nitroglycerin (NTG) [endothelium-independent, NTG-induced dilatation (NID)] at Gestational Weeks 11 and 29. Plasma concentrations of the vascular markers vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor antigen were also measured together with 24-h urinary albumin excretion (UAE), blood pressure (BP), and HbA(1C).
Fourteen (17%) of the 83 women developed preeclampsia. NID was significantly impaired at Week 29 in women prone to preeclampsia (108.8+/-7.0% vs. 116.8+/-8.9%, mean+/-S.D., P<.05), and the plasma concentrations of VCAM-1 and ICAM-1 were significantly elevated at Gestational Week 11 (612+/-82 vs. 516+/-109 microg/l, P<.005 and 293+/-67 vs. 255+/-57 microg/l, P<.05, respectively). Women who later developed preeclampsia were also characterized by higher UAE, higher BP, and higher HbA(1C) than women who did not [Gestational Week 11: 194 (3-1104) vs. 7 (0-412) mg/24 h, median (range), P=.0003; 122+/-12/75+/-6 vs. 111+/-11/69+/-9 mmHg, mean+/-S.D., P<.01; and 8.2% (5.9-10.5%) vs. 7.2% (5.3-10.9%), P=.008, respectively].
This prospective study indicates that signs of maternal vascular dysfunction precede development of preeclampsia in women with type 1 diabetes.
本研究旨在验证如下假设，即1型糖尿病且随后发生先兆子痫的女性在妊娠早期即存在血管功能障碍。
对83例病程超过10年的1型糖尿病女性患者进行孕期前瞻性随访。在妊娠第11周和第29周时，采用体外超声测量肱动脉对缺血后血流增加的扩张反应（内皮依赖性、血流相关扩张）以及对硝酸甘油（NTG）的反应[非内皮依赖性、NTG诱导扩张（NID）]。同时还检测了血管标志物血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-1）、E-选择素和血管性血友病因子抗原的血浆浓度，以及24小时尿白蛋白排泄量（UAE）、血压（BP）和糖化血红蛋白（HbA1C）。
83例女性中有14例（17%）发生了先兆子痫。易发生先兆子痫的女性在第29周时NID明显受损（108.8±7.0%对116.8±8.9%，均值±标准差，P<0.05），且在妊娠第11周时VCAM-1和ICAM-1的血浆浓度显著升高（分别为612±82对516±109μg/l，P<0.005；293±67对255±57μg/l，P<0.05）。与未发生先兆子痫的女性相比，后来发生先兆子痫的女性还具有更高的UAE、更高的BP和更高的HbA1C[妊娠第11周：194（3 - 1104）对7（0 - 412）mg/24 h，中位数（范围），P = 0.0003；122±12/75±6对111±11/69±9 mmHg，均值±标准差，P<0.01；以及8.2%（5.9 - 10.5%）对7.2%（5.3 - 10.9%），P = 0.008]。
这项前瞻性研究表明，1型糖尿病女性先兆子痫发生之前就存在母体血管功能障碍的迹象。
