Preeclampsia

Abstract

Hypertensive disorders of pregnancy—chronic hypertension, gestational hypertension, and preeclampsia—are uniquely challenging as the pathology and its therapeutic management simultaneously affect mother and fetus, sometimes putting their well-being at odds with each other. Preeclampsia, in particular, is one of the most feared complications of pregnancy. Often presenting as new-onset hypertension and proteinuria during the third trimester, preeclampsia can progress rapidly to serious complications, including death of both mother and fetus. While the cause of preeclampsia is still debated, clinical and pathological studies suggest that the placenta is central to the pathogenesis of this syndrome. In this review, we will discuss the current evidence for the role of abnormal placentation and the role of placental factors such as the antiangiogenic factor, sFLT1 (soluble fms-like tyrosine kinase 1) in the pathogenesis of the maternal syndrome of preeclampsia. We will discuss angiogenic biomarker assays for disease-risk stratification and for the development of therapeutic strategies targeting the angiogenic pathway. Finally, we will review the substantial long-term cardiovascular and metabolic risks to mothers and children associated with gestational hypertensive disorders, in particular, preterm preeclampsia, and the need for an increased focus on interventional studies during the asymptomatic phase to delay the onset of cardiovascular disease in women.

Potential Role of Circulating Endoglin in Hypertension via the Upregulated Expression of BMP4

“…Interestingly, endothelial dysfunction precedes and mediates the BMP4-induced hypertensive effect [60,61,77]. This is in agreement with the presence of a generalized endothelial dysfunction in preeclampsia likely due to placental factors such as sEng [41,42,58,69]; syncytiotrophoblasts being the major source of sEng [17,38]. In fact, it has been reported that sEng contributes to endothelial dysfunction.…”

“…Abnormally elevated levels of sEng have been found in several vascular-related pathologies [6,37,38], including preeclampsia, a multisystem disorder of high prevalence in pregnant women marked by the onset of hypertension, proteinuria or systemic endothelial dysfunction. If left untreated, preeclampsia can lead to serious, even fatal, complications for both mother and baby [41,42]. Noteworthy, several lines of evidence support a pathogenic role of sEng in cardiovascular conditions and diseases, including hypertension, endothelial dysfunction, anti-angiogenic activity, increased vascular permeability, vascular remodeling, and inflammation-associated leukocyte adhesion and transmigration [14,15,33,34,[42][43][44][45].…”

Cerebrospinal beta-amyloid peptides(1-40) and (1-42) in severe preeclampsia and HELLP syndrome – a pilot study

“…We are aware that routine lumbar puncture for diagnosis of PE and HELLP syndrome is not practical during pregnancy. Furthermore, treatment is limited mostly to maternal stabilization and timely delivery by medically induced labor or cesarean section 2 . In women with PE and HELLP syndrome delivery by cesarean section was on average four weeks of gestation earlier than in controls, thus partly explaining the low values for placental weight, baby weight and Apgar score.…”

Coenzyme Q10: Clinical Applications in Cardiovascular Diseases

“…However, in some cases, there is worsening of preexisting hypertension, generalized edema, proteinuria (300 mg/L or more in 24 h), and sometimes blood clotting disorders that arise after 20 weeks of gestation [161]. Oxidative stress could be one of the causing factors of this dangerous condition [162]. From one side, pregnant women with established pre-eclampsia have significantly lower plasma levels of CoQ 10 compared to healthy pregnant women [163,164].…”