Prediction and prevention of hypertensive disorders of pregnancy

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.

Markedly higher sFlt‐1/PlGF ratio in a woman with acute fatty liver of pregnancy compared with HELLP syndrome

“…In women with HELLP syndrome, the levels of sFlt‐1 were all less than 100 000 pg/mL. Because the abnormality of sFlt‐1 levels in pregnancy is related to endothelial dysfunction in pre‐eclampsia, the markedly increased levels of sFlt‐1 in our AFLP patient might have reflected severer endothelial dysfunction underlying this condition, and thereby might have been associated with the genesis of liver dysfunction, renal dysfunction, low AT activity and thrombocytopenia, and also associated with the slow amelioration of all these abnormalities.…”

Maternal plasma kisspeptin‐10 level in preeclamptic pregnant women and its relation in changing their reproductive hormones

“…Numerous mechanisms have been proposed to account for the clinical presentation of PE, but the underlying pathophysiology remains unclear. As such, while vascular dysfunction may play a role in the pathophysiology of PE, the etiology appears more likely to be the consequence of abnormal trophoblast invasion leading to the inappropriate physiological conversion of the spiral arteries and, hence, the impaired placental function …”

“…As such, while vascular dysfunction may play a role in the pathophysiology of PE, the etiology appears more likely to be the consequence of abnormal trophoblast invasion leading to the inappropriate physiological conversion of the spiral arteries and, hence, the impaired placental function. 2,3 Many pathophysiological factors have been implicated in trophoblast invasion, including endogenous peptides. Such as kisspeptin (145 amino acid peptide) an endogenous peptide that is encoded by the KiSS1 gene in humans and its ligand G-protein coupled receptor 54 (GPR54), which are together expressed in the placenta of normal pregnant woman.…”

Fetal Biparietal Diameter as a Potential Risk Factor for Emergency Cesarean Section due to Labor Arrest

“…A diagnosis of GDM was made if there was at least one abnormal plasma glucose value (≥ 92, 180, and 153 mg/dL among fasting, 1-h, and 2-h plasma glucose concentrations, respectively) after a 75-g oral glucose tolerance test (Minakami et al 2014). HDP was defined as a blood pressure level ≥ 140/90 mmHg on at least two occasions (Ohkuchi et al 2017). In a previous study, short stature was defined by a cut-off value at the 5 th percentile ranking (Toh-Adam et al 2012) and was consequently defined as height < 150 cm in this study.…”