Preeclampsia: long-term consequences for vascular health

Abstract

Preeclampsia (PE) is a pregnancy-specific syndrome and one of the leading causes of preterm birth, neonatal and maternal morbidity and mortality. This disease is characterized by new onset hypertension usually in the third trimester of pregnancy and is sometimes associated with proteinuria, although proteinuria is not a requirement for the diagnosis of PE. In developing countries, women have a higher risk of death due to PE than more affluent countries and one of the most frequent causes of death is high blood pressure and stroke. Although PE only affects approximately 2%–8% of pregnancies worldwide it is associated with severe complications such as eclampsia, hemorrhagic stroke, hemolysis, elevated liver enzymes and low platelets (HELLP syndrome), renal failure and pulmonary edema. Importantly, there is no “cure” for the disease except for early delivery of the baby and placenta, leaving PE a health care risk for babies born from PE moms. In addition, PE is linked to the development of cardiovascular disease and stroke in women after reproductive age, leaving PE a risk factor for long-term health in women. This review will highlight factors implicated in the pathophysiology of PE that may contribute to long-term effects in women with preeclamptic pregnancies.

PZP and PAI-2: Structurally-diverse, functionally similar pregnancy proteins?

“…Substantial evidence supports the conclusion that enhanced Th1 cell activity is important in the pathology of preeclampsia (Amaral et al, 2015). Both α 2 M and PZP are reported to potentiate the ability of PP14 to inhibit Th1 cells, but comparatively, PZP appears to be more efficient at performing this role (Skornicka et al, 2004) (Fig.…”

“…Preeclampsia is a leading cause of maternal and neonatal morbidity and mortality with currently unknown etiology. The disorder is characterised by high maternal blood pressure, proteinuria, aberrant placental development and haemostatic and fibrinolytic disturbances (Hunt et al, 2009, Amaral et al, 2015. It is known that PZP levels vary markedly between individuals (Ekelund and Laurell, 1994).…”

“…Systemic inflammation in preeclampsia is much greater than that which occurs in normal pregnancy (Amaral et al, 2015), and it has been proposed that increased myeloperoxidase (the enzyme that generates hypochlorite) in blood plasma and the placenta is an important source of oxidative stress in preeclampsia (Gandley et al, 2008). An increased PAI-1/PAI-2 ratio and placental oxidative stress have been reported as good predictors of preeclampsia (Wikstrom et al, 2009).…”

Relationship Between Clinical, Placentary, Obstetric and Neonatal Aspects and Intrauterine Growth in High Risk Pregnancies

“…2 Although the human placenta is a vital organ for maintaining pregnancy and promoting normal fetal development, 3 a pattern of morphological alteration found may indicate maternal and fetal clinical involvement related to gestational hypertensive syndromes, 4 to intrauterine growth restriction (IUGR), 5 to Diabetes Mellitus (DM) or to placental abruption (PA), with small for gestational age (SGA) newborns, 5 decreased placental flow (placental hypoxia) or miscarriage resulting as a consequence. 6 Aggressions involving the uterine-placental unit may divert the fetus from its genetic growth potentia, 7 resulting in a condition known as IUGR 5 (Intrauterine Growth Restriction) and in complications related to a higher incidence of fetal distress, the presence of meconial amniotic fluid, low Apgar score, low birth weight (LBW) and perinatal death. 3 Intrauterine growth deviations (IUGDs) are associated with perinatal morbidity and mortality, and the risk of developing diseases in adult life such as DM and cardiovascular diseases.…”

Nouveaux regards sur la prééclampsie

“…de la pression artérielle chez les enfants ayant vécu ce type de grossesse [8]. Sept années après avoir souffert d'une PE, 20 % des femmes présentent une hypertension et une protéinurie (traduisant une altération rénale).…”