Antiphospholipid syndrome and pregnancy

Abstract

The reasons behind vascular thrombosis are still unclear. The “two hit” hypothesis suggests that the “first hit” may be oxidative stress, surgery, trauma, or infections leading to endothelia cell damage. This exerts different effects on endothelial cells, monocytes, platelets, and complement. Binding and activation of these cell types causes an increased expression of adhesion molecules, secretion of cytokines, and production of arachidonic acid metabolites. aPL may also participate in oxidant-mediated injury to vascular endothelium or bind to perturbed cells that lose their regular membrane symmetry and express anionic phospholipids on their surface. The interaction of antibodies with clotting regulation such as prothrombin, factor X, protein C, and plasmin might hinder inactivation of procoagulant factors and impede fibrinolysis. In pregnancy, placental thrombosis and fetal loss may result from interference with annexin A5, a natural anticoagulant. Abnormalities in placentation leading to pregnancy loss may result from antibodies binding leading to a reduction of human chorionic gonadotropin secretion or triggering an inflammatory response resulting in trophoblast damage.6