“…5,6 Biological evidence of endothelial dysfunction has been shown by increased plasma levels of markers including fibronectin, von Willebrand factor, ICAM-1, VCAM-1, and E-selectin. 6,[8][9][10][11] Recently, a new marker or causative agent of RM is discussed: the cell-derived circulating microparticles (cMP). In cases of RM associated with aPL, the main thrombogenic mechanism includes other pathways: interference with coagulation soluble factors -protein C pathway inhibition, antithrombin III (ATIII) inhibition, annexin A5 displacement, blocking of the anticoagulant activity of b 2 GP1, monocyte activation with tissue factor up-regulation, endothelial dysfunction, and fibrinolysis impairment.…”