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Pregnancy Hypertens ; 34: 13-18, 2023 Dec.
Article in English | MEDLINE | ID: mdl-37778280

ABSTRACT

OBJECTIVE: To determine the optimal cutoff value for the soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio to predict maternal and fetal adverse events in pregnancies with uterine artery Doppler scans results above the 95th percentile in the late second trimester. STUDY DESIGN: Retrospective, observational cohort study on 116 asyntomatic patients with abnormal uterine artery Doppler scans at gestational week 25. The sFlt-1/PlGF ratio was determined within the weeks 25 to 29 of gestation and ROC curve analysis performed. The diagnostic validity of different cutoff values to predict severe maternal and fetal complications, i.e. preeclampsia, fetal growth restriction, placental abruption, and fetal death, was analyzed. MAIN OUTCOME MEASURES: An ideal cutoff for sFlt-1/PlGF ratios in pregnancies with abnormal uterine artery Doppler in the second trimester. RESULTS: Applying a cutoff point of 38, the area under the ROC curve was 0.89, generally considered low risk in fetal and maternal complication prediction. The sensitivity was 32.1%, the specificity 98.4%, the positive predictive value (PPV) 94.4%, and the negative predictive value (NPV) 63.3%. A cutoff value of 10, leading to the highest Youden index, performed best at detecting overall complications, increasing sensitivity to 69.8% and the NPV to 76.8%. at the cost of a reduced specificity and PPV. CONCLUSIONS: In pregnancies with abnormal uterine artery Doppler in the second trimester, an sFlt-1/PlGF cutoff value greater than equal to 38 improves its predictive power for adverse events.


Subject(s)
Pre-Eclampsia , Pregnancy , Female , Humans , Pregnancy Trimester, Second , Placenta Growth Factor , Retrospective Studies , Pre-Eclampsia/diagnostic imaging , Uterine Artery/diagnostic imaging , Uterine Artery/metabolism , Placenta/metabolism , Biomarkers , Predictive Value of Tests , Rheology , Vascular Endothelial Growth Factor Receptor-1/metabolism
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