Abstract

The most common classifications of hypertensive disorders of pregnancy consist of chronic hypertension, gestational hypertension, preeclampsia (PE) and superimposed PE. A common final pathophysiology of PE is endothelial dysfunction. The most successful translational research model for explaining the cause-effect relationship in the genesis of PE is the angiogenic/angiostatic balance theory, involving soluble fms-like tyrosine kinase 1 (sFlt-1), placental growth factor (PlGF) and soluble endoglin (sEng). In a systematic review of articles on the prediction of early-onset PE using angiogenesis-related factors, we revealed that the prediction of early-onset PE in the first trimester is clinically possible, but the prediction of early-onset PE in the early third trimester might be ideal. In addition, an onset threshold or a serial approach appeared to be clinically useful for predicting the imminent onset of PE, with onset at <4 weeks after blood sampling in the second and early third trimesters, because the positive likelihood ratio was >10 and the positive predictive value was >20%. The National Institute for Health and Care Excellence guidelines state that the Triage PlGF testing and Elecsys immunoassay for the sFlt-1/PlGF ratio could help to exclude PE in women with suspected PE at 20-34 weeks of gestation. Until now, we have not found any effective therapies to prevent PE. However, low-dose aspirin treatment starting at ⩽16 weeks of gestation might be associated with a marked reduction in PE. In addition, early statin treatment might prevent the occurrence of PE. Currently, a clinical trial using pravastatin for the prevention of PE is ongoing.

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