Personalized hemostasis correction in recurrent pregnancy loss: analysis of current data, clinical controversies, and prospects

Aim : to systematize current evidence and analyze the effectiveness of personalized approaches to correcting hemostatic disorders for preventing recurrent pregnancy loss and placenta-mediated complications. Materials and Methods . A systematic search for publications from 1999 to 2025 was conducted in PubMed/MEDLINE, eLibrary, CyberLeninka, DOAJ (for scientific articles) and FIPS (for patent documents) databases. Using combined MeSH queries, 412 records were initially identified. After removing duplicates and performing multi-stage screening, 63 full-text publications were included in the final analysis. Due to clinical and methodological heterogeneity across studies, a qualitative narrative synthesis of the data was performed. Results . Hemostatic dysregulation serves as a universal pathogenetic arm in pregnancy loss, manifesting through chorionic villi microthrombosis and placental dysfunction. The combination of acetylsalicylic acid (ASA) 100–150 mg and prophylactic doses of low-molecular-weight heparins (LMWHs) significantly increases live birth rates in antiphospholipid syndrome. It is emphasized that isolated carriage of thrombophilia gene polymorphisms is not an independent indication for LMWHs; their use is pathogenetically and clinically justified only when combined with additional risk factors, such as verified antiphospholipid syndrome (APS), a history of thrombosis, or multiple pregnancy losses. For primary preeclampsia prevention, ASA efficacy at 150 mg initiated at 11–14 weeks of gestational age is well established. The critical importance of preconception administration of active folates for hyperhomocysteinemia correction is confirmed. Integral monitoring via thrombodynamics enables tracking of trimester-specific coagulation changes and personalizing antithrombotic dosing. Sulodexide and dipyridamole demonstrate clinical potential in improving uteroplacental blood flow in fetoplacental insufficiency. Conclusion . The contemporary management paradigm for these patients requires a shift from empirical regimens to risk stratification and early preconception screening. Optimal clinical strategy is based on evidence-based ASA prescription, strictly differentiated use of LMWHs, folate metabolism correction, and dynamic therapy control using thrombodynamics. The presented data will help minimize iatrogenic complications and define the trajectory for future multicenter studies.