[Pathophysiology and clinical manifestations in pre-eclampsia]

Area of Science:

• Obstetrics and Gynecology
• Maternal-Fetal Medicine
• Pathophysiology

Context:

• Preeclampsia is a serious pregnancy complication characterized by hypertension and proteinuria.
• Evidence suggests a genetic predisposition and placental pathology as central to preeclampsia.
• Existing literature reviews highlight the need for deeper understanding of preeclampsia's mechanisms.

Purpose:

• To review the current understanding of preeclampsia's pathophysiology.
• To synthesize findings on placental dysfunction, endothelial damage, and metabolic factors in preeclampsia.
• To explore the role of genetic factors and coagulation abnormalities in severe and early-onset preeclampsia.

Summary:

• Defective placental development and invasion of spiral arteries lead to poor placental perfusion, hypoxia, and cytokine release, causing endothelial dysfunction.
• Elevated triglyceride-rich lipoproteins and lipid peroxidation, originating partly from the placenta, contribute to endothelial damage and preeclampsia.
• Factors such as antioxidant deficiency, hyperhomocysteinemia, and deficiencies/resistance in proteins S and C are implicated in severe and early-onset preeclampsia.

Impact:

• Advances in understanding preeclampsia pathophysiology can inform the development of novel therapeutic strategies.
• This review provides a foundation for future research into targeted treatments for preeclampsia.
• Improved knowledge of preeclampsia mechanisms may lead to better patient outcomes and reduced maternal-fetal morbidity.