Updates on Preeclampsia: Pathogenesis, Biomarkers, Diagnosis, and Management

Preeclampsia complicates 2-4% of pregnancies globally and contributes significantly to maternal and fetal morbidity and mortality. Early-onset preeclampsia (<34 weeks gestation) is primarily characterized by abnormal placentation and defective remodeling of uterine spiral arteries, while late-onset preeclampsia (>34 weeks gestation) often involves a mismatch between normal maternal perfusion and increasing placental metabolic demands. Angiogenic imbalance, featuring elevated antiangiogenic factors [soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin] and decreased proangiogenic factors [placental growth factor (PlGF)], plays a pivotal role in disease manifestation. Diagnostic criteria include hypertension with new-onset proteinuria, maternal end-organ damage, or uteroplacental dysfunction. The addition of sFlt-1/PlGF ratio has been Food and Drug Administration approved for risk assessment for preeclampsia. Prevention strategy includes mainly low-dose aspirin for high-risk women. While delivery remains the definitive treatment, novel therapies targeting the pathophysiology of preeclampsia are being investigated, including therapeutic apheresis, siRNA therapies, metformin, proton pump inhibitors, statins, and complement inhibitors. Women with a preeclampsia history face significantly increased long-term risks of cardiovascular disease, stroke, renal dysfunction, and metabolic disorders, emphasizing the need for comprehensive postpregnancy follow-up and preventive strategies. This review comprehensively examines the pathogenesis, diagnosis, biomarkers, and management strategies of preeclampsia.