MOLECULAR MECHANISMS OF OBSTETRIC ANTIPHOSPHOLIPID SYNDROME

Antiphospholipid syndrome is an autoimmune disease marked by antiphospholipid antibodies, causing thrombosis and obstetric complications.

This study explores molecular mechanisms, endometrial receptivity, and clinical parameters linked to APS, focusing on pregnancy complications such as miscarriage, preterm delivery, recurrent implantation failure (RIF), and thrombosis.

A systematic review was conducted through Scopus, WoS, PubMed, Cochrane, and Google Scholar, including studies published between 2019 and 2024. 17 relevant original research studies were selected, focusing on clinical trials and observational studies. Narrative reviews and meta-analyses were excluded, with priority given to preeclampsia-specific studies to explore the immune and vascular dysfunction link in APS patients.

Key findings include the correlations between elevated antiphospholipid antibodies (aPLs), including aCL and aβ2GPI, poor vascularization of the uterus, and recurrent pregnancy loss (RPL) reports. Preeclampsia is closely linked to APS, resulting in immune and vascular dysfunctions that exacerbate complications, including miscarriage, preterm delivery, and fetal death. ELISA, Doppler ultrasound, and genetic testing are some of the diagnostic methods applied. The aPL autoantibodies along with inflammatory markers like CRP and TNFSF13B, an increase in cytokine imbalance, are associated with many pregnancy complications such as early-stage miscarriage and preterm delivery. Deficient inflammation resolution and adequate uterine perfusion, abnormal uterine blood perfusion, and chronic infection significantly impact rates of perinatal illness and death which emphasizes the problem in identifying and managing APS.

This review focuses on the effects of the antiphospholipid syndrome on the endometrial receptivity and pregnancy outcomes, paying special attention to how early diagnosis and treatment can enhance the chances of a successful pregnancy and reduce complications.