Pathophysiology of Placenta in Antiphospholipid Syndrome

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by clinical manifestations caused arterial or venous thrombosis and pregnancy conditions such as recurrent miscarriage, fetal death, premature birth in the presence of antiphospholipid antibodies. The obstetrical are strongly related to placental alterations. aim this review summarize latest data on pathophysiology APS, emphasizing disturbance placentation process. Due a lack extravillous trophoblasts properly reconstruct spiral arteries, APS causes hypoxic ischemic injury high-speed blood flow that damages placenta. This results decreased interrupted maternal placenta nutrients for fetus. antibodies can lower proliferation infiltration trophoblasts. mal-perfusion release antiangiogenic substances soluble fms-like tyrosine kinase-1 endoglin. Placental growth factor vascular endothelial (VEGF) may be sequestered sFlt1 blocked from binding trophoblast cell VEGF receptors, inhibiting their proangiogenic effects. Preeclampsia result angiogenic factors needed homeostasis due excess circulation.