Abstract
BackgroundDifferences in circulating concentrations of antiangiogenic factors sFlt1 and soluble endoglin (sEng) and the pro-angiogenic growth factor PlGF are reported to precede the onset of preeclampsia weeks to months in low-risk pregnant women. The objective of this study was to investigate whether similar changes can be detected in pregnant women at high-risk to develop the syndrome.MethodsThis study is a secondary analysis of the NICHD MFMU trial of aspirin to prevent preeclampsia in high-risk pregnancies. Serum samples were available from 194 women with pre-existing diabetes, 313 with chronic hypertension, 234 with multifetal gestation, and 252 with a history of preeclampsia in a previous pregnancy. Samples collected across pregnancy were analyzed in a blinded fashion for sFlt1, sEng and PlGF.ResultsThe odds of developing preeclampsia were significantly increased among women with multiple fetuses for each 2-fold elevation in sFlt1, sEng and the ratio of angiogenic factors (e.g. OR 2.18, 95% CI 1.46-3.32), and significantly decreased for each 2-fold elevation in circulating PlGF (OR 0.50, 95% CI 0.30-0.82) between 7 and 26 weeks' gestation. Cross-sectional analysis of the angiogenic factors across gestation showed significant differences during the third trimester in women who develop preeclampsia compared with appropriate controls in all high-risk groups. However, when data were examined in relation to the gestational week when preeclampsia was diagnosed only sFlt1 was significantly higher 2 to 5 weeks before the clinical onset of preeclampsia and only in women with previous preeclampsia.ConclusionsThe pattern of elevated concentrations of sFlt1 and sEng, and low PlGF in high-risk pregnant subjects who develop preeclampsia is similar to that reported in low-risk pregnant women. However, differences in these factors among high-risk women who do and do not develop preeclampsia are modest, and do not appear to be clinically useful predictors in these high-risk pregnant women.
Highlights
Preeclampsia is a pregnancy-specific syndrome affecting approximately 5% of all pregnancies and is a leading cause of maternal and fetal morbidity and mortality worldwide [1,2,3]
The pathogenesis of preeclampsia remains incompletely elucidated, increased attention has been directed toward the role of angiogenic and antiangiogenic factors including elevated soluble fms-like tyrosine kinase 1 and soluble endoglin, and lower placental growth factor (PlGF) [5,6,7,8]
The goal of this study was to investigate whether differences in the angiogenic factors soluble fms-like tyrosine kinase 1 (sFlt1), soluble endoglin (sEng) and PlGF in high-risk patients would identify women who later develop preeclampsia in a manner similar to reports in the literature regarding low-risk women
Summary
Preeclampsia is a pregnancy-specific syndrome affecting approximately 5% of all pregnancies and is a leading cause of maternal and fetal morbidity and mortality worldwide [1,2,3]. The pathogenesis of preeclampsia remains incompletely elucidated, increased attention has been directed toward the role of angiogenic and antiangiogenic factors including elevated soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng, a receptor for members of the TGFb superfamily), and lower placental growth factor (PlGF) [5,6,7,8] Concentrations of these factors are significantly different in low-risk women who later develop preeclampsia several weeks to months before clinical manifestations of the disorder when compared with similar lowrisk women who have uncomplicated pregnancies [6,9]. The high-risk groups studied in this secondary analysis, chronic hypertensive, prepregnancy diabetes, women with multifetal gestation, or previous preeclampsia, were analyzed separately following a pre-analysis hypothesis that the pathogenesis of preeclampsia for each group may be different This permitted investigation of possible differences in angiogenic factor levels between the groups. The objective of this study was to investigate whether similar changes can be detected in pregnant women at highrisk to develop the syndrome
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