Previous evidence has suggested that placental dysfunction
, which includes pre-eclampsia, is passed from mother to daughter.
Cytomegalovirus infection of trophoblast cells elicits an inflammatory response: a possible mechanism of placental dysfunction
. Am J Obstet Gynecol.
can seriously affect fetal growth, development and maintenance of pregnancy14.
Knowledge of maternal circulating concentration of Placental Growth Factor, PLGF, a biomarker for placental dysfunction
, aids in the early and accurate diagnosis of preterm pre-eclampsia and helps clinicians to accurately risk-stratify pregnant women resulting in more efficient use of healthcare resources and the potential for cost-saving to the healthcare system.
It is reasonable to assume that if placental dysfunction
compromises a fetus, body movements are reduced in an effort to conserve energy.
The pathogenesis includes placental dysfunction
which is characterised by defective trophoblastic invasion and incomplete physiological remodelling of myometrial spiral arteries during the first 20 weeks of gestation (8).
I postulate that: Pre-natal exposure to urban air pollution during pregnancy impairs foetal and postnatal brain development, Mainly by affecting myelination; These effects are at least partially mediated by translocation of airborne particulate matter to the placenta and by placental dysfunction
; And prenatal exposure to air pollution impairs post-natal brain development independently of urban context and post-natal exposure to air pollution.
Both of these can contribute to a greater risk for complications such as multiple gestation, chromosomal and congenital abnormalities in the fetus, stillbirth and placental dysfunction
and gestational diabetes or hypertensive disorders of pregnancy.
In the case of preeclampsia and placental dysfunction
, the amount of necrotic and apoptotic-altered trophoblast cells increases.
PAPP-A is a marker of placental syncitiotrophoblasts and reduced serum levels may serve as a marker for early placental dysfunction
The well-known pathophysiological mechanism of HELLP syndrome is based on the release of various placental factors such as soluble vascular endothelial growth factor receptor-1 (sVEGFR-1), which then binds vascular endothelial growth factor (VEGF) and placental growth factor (PGF), causing endothelial cell and placental dysfunction
by preventing them from binding to endothelial cell receptors.
This heightened state of placental inflammation can lead to placental dysfunction
, including the development of insulin resistance, excessive amino acid, and free fatty acid delivery to the fetus or reduced mitochondrial respiration and ATP generation [20-22].