Hypertensive disorders of pregnancy (HDPs) affect 2%-8% of pregnancies globally. Of HDPs, preeclampsia contributes the most to adverse maternal and perinatal outcomes.
Preeclampsia is characterised by the development of new-onset hypertension and proteinuria after 20 weeks of gestation, although proteinuria is no longer a necessary diagnostic requirement. It is a multi-factorial disorder that manifests with systemic endothelial dysfunction in various organs.
MATERNAL AND PERINATAL OUTCOMES
Preeclampsia contributes significantly to maternal and perinatal morbidity and mortality. The definition of preeclampsia is constantly evolving.
Preeclampsia is a leading cause of maternal and perinatal morbidity and mortality, more so in low-to-middle-income countries (LMICs).
The burden on the healthcare system includes:
- Antenatal: surveillance, confirmation of diagnosis, conservative management
- Perinatal: management of maternal complications (resuscitation and ICU) and iatrogenic preterm delivery – implications on NICU and neurodevelopment
- Postnatal: prolonged in-hospital stay
- Maternal:-downstream cardiovascular health
- Foetal: effects on placental programming and increased risk for non-communicable disease.
The pathophysiology of preeclampsia has been evolving since ancient times and remains a subject of research. Pathophysiology is likely influenced by placental and maternal contributory factors. Placental factors involve compromised trophoblast invasion and transformation of the spiral arteries.
Maternal contributory factors are complex and may include genetic predisposition, immune intolerance and auto-immunity and compromised vascular health. It is important to recognise that molecular pathways implicated in the pathophysiology of preeclampsia are diverse.
The following angiogenic factors have been extensively studied:
- PLGF
- VEGF
- Solublefms-like tyrosine kinase-1 (sFlt-1)
- Soluble Endoglin (sEng).
PROPOSED SFLT-1 MECHANISMS IN PATHOGENESIS OF PREECLAMPSIA
VEGF, PlGF and sFlt-1 may be involved in the mesothelial-endothelial adhesion profile transition required for successful trophoblast invasion (pseudovasculogenesis) (Zhou).
Exogenous sFlt-1 inhibits cytotrophoblast invasion. There is direct maternal endothelial disruption resulting in systemic endothelial manifestations in different organs.
Pro-angiogenic ligands (VEGF-A and PlGF) are diminished in PET and anti-angiogenic (sFlt-1) is elevated. Angiogenic biomarkers predate the clinical syndrome and may have a role in early prediction, risk assessment and management (with potential cost-saving implications from the reduction in hospitalisation). Angiogenic biomarkers are not to be used in isolation but interpreted in conjunction with clinical and biochemical assessments.
CONCLUSION
Making novel impacts on preeclampsia will require a thorough understanding of disease epidemiology and pathophysiology.
Angiogenic biomarkers contribute to pathophysiological understanding and are likely to revolutionise the classification and management of PET.
Further investment in research (within LMICs) aimed at understanding pathophysiological mechanisms is paramount. The developing world bears the brunt of severe disease and adverse maternal and perinatal outcomes.
About 99% of the estimated annual global maternal and perinatal pre-eclampsia-related deaths occur in LMICs.
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