Wantania John, Attamimi Ahsanuddin, Siswishanto Rukmono
Associate Professor, Department of Obstetric and Gynaecology, Maternal Foetal Medicine Division, Medical Faculty, Sam Ratulangi University, Manado, Indonesia.
Assistant Professor, Department of Obstetric and Gynaecology, Maternal Foetal Medicine Division, Medical Faculty, Gadjah Mada University, Yogyakarta, Indonesia.
J Clin Diagn Res. 2017 Mar;11(3):QC35-QC38. doi: 10.7860/JCDR/2017/21516.9603. Epub 2017 Mar 1.
Preeclampsia is a pregnancy complication characterized by high blood pressure and proteinuria. Endothelial dysfunction is a major theory suggested as its aetiology. It is caused by anti-angiogenic condition characterized by low Vascular Endothelial Growth Factor (VEGF). An estradiol metabolite, called 2-Methoxy Estradiol (2-ME), is produced with the help of Catechol-O-Methyltransferase (COMT). This substance has an important role in VEGF expression. A 2-ME is suppressed in women with preeclampsia.
To compare 2-ME in women with severe preeclampsia and normotensive pregnancy.
A total of 80 subjects qualified the inclusion and exclusion criteria, were divided into two groups (40 each): the severe preeclampsia and the normotensive pregnancy. Blood sample was collected and examined with the ELISA 2-ME kit (Cayman). The data were compared and calculated using Fisher-Exact test to examine 2-ME differences between the two groups.
Women age, parity, and gestational age showed a non significant difference between both groups. Nonetheless, the BMI before pregnancy and the history of preeclampsia in the past pregnancy showed significant differences. In this study, the 2-ME value was lower in the severe preeclampsia group compared to the normotensive.
This study concludes that 2-ME value in severe preeclampsia is lower than normotensive pregnancy. A lower 2-ME value may indicate COMT not producing enough 2-ME which in turn may cause the pre-eclampsia.
子痫前期是一种以高血压和蛋白尿为特征的妊娠并发症。内皮功能障碍是其病因的主要理论。它由以低血管内皮生长因子(VEGF)为特征的抗血管生成状态引起。一种名为2-甲氧基雌二醇(2-ME)的雌二醇代谢产物是在儿茶酚-O-甲基转移酶(COMT)的帮助下产生的。这种物质在VEGF表达中起重要作用。子痫前期女性中2-ME受到抑制。
比较重度子痫前期女性和血压正常孕妇的2-ME水平。
共有80名符合纳入和排除标准的受试者被分为两组(每组40人):重度子痫前期组和血压正常妊娠组。采集血样并用ELISA 2-ME试剂盒(开曼)进行检测。使用Fisher精确检验对数据进行比较和计算,以检验两组之间2-ME的差异。
两组女性的年龄、产次和孕周无显著差异。然而,孕前体重指数和既往妊娠子痫前期病史存在显著差异。在本研究中,重度子痫前期组的2-ME值低于血压正常组。
本研究得出结论,重度子痫前期的2-ME值低于血压正常妊娠。较低的2-ME值可能表明COMT产生的2-ME不足,进而可能导致子痫前期。