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Revista Brasileira de Ginecologia e Obstetrícia. 2018;40(10):593-598
To analyze endocan-1, a biomarker of vascular endothelial related pathologies, and the placental growth factor (PlGF), an angiogenic factor and a placental dysfunction marker in patients with preeclampsia (PE).
Case-control study conducted at Hospital São Lucas, in the city of Porto Alegre, Brazil. Endocan-1 and PlGF levels were quantified in the maternal plasma using the MagPlexTH-C microsphere system (MAGPIX System, Luminex, Austin, Texas, US) and evaluated through analysis of covariance (ANCOVA) and adjusted by body mass index (BMI), gestational age and maternal age. To estimate the difference between the groups, the mean ratio (MR) and the 95% confidence interval (95%CI) were calculated. The Pearson correlation test was used to establish any association between endocan-1 and PlGF levels. The null hypothesis was rejected when p < 0.05.
The group of patients was composed by normotensive (n = 67) patients and patients with PE (n = 50). A negative correlation between endocan-1 and the PlGF was noted in the entire normotensive group (linear correlation coefficient [r] = -0.605; p < 0.001), as well as in the PE group (r = -0.545; p < 0.001).
Endocan-1 levels are increased in patients with PE, and are inversely correlated with PlGF levels. We suggest that it is important to analyze angiogenic and proinflammatory molecules concomitantly in women with PE to better understand the pathophysiology of the disease. Both molecules are strong candidates for PE biomarkers, and future studies will examine any mechanisms connecting these factors in PE.
Summary
Revista Brasileira de Ginecologia e Obstetrícia. 2018;40(10):593-598
To analyze endocan-1, a biomarker of vascular endothelial related pathologies, and the placental growth factor (PlGF), an angiogenic factor and a placental dysfunction marker in patients with preeclampsia (PE).
Case-control study conducted at Hospital São Lucas, in the city of Porto Alegre, Brazil. Endocan-1 and PlGF levels were quantified in the maternal plasma using the MagPlexTH-C microsphere system (MAGPIX System, Luminex, Austin, Texas, US) and evaluated through analysis of covariance (ANCOVA) and adjusted by body mass index (BMI), gestational age and maternal age. To estimate the difference between the groups, the mean ratio (MR) and the 95% confidence interval (95%CI) were calculated. The Pearson correlation test was used to establish any association between endocan-1 and PlGF levels. The null hypothesis was rejected when p < 0.05.
The group of patients was composed by normotensive (n = 67) patients and patients with PE (n = 50). A negative correlation between endocan-1 and the PlGF was noted in the entire normotensive group (linear correlation coefficient [r] = -0.605; p < 0.001), as well as in the PE group (r = -0.545; p < 0.001).
Endocan-1 levels are increased in patients with PE, and are inversely correlated with PlGF levels. We suggest that it is important to analyze angiogenic and proinflammatory molecules concomitantly in women with PE to better understand the pathophysiology of the disease. Both molecules are strong candidates for PE biomarkers, and future studies will examine any mechanisms connecting these factors in PE.
