Systemic endothelial cell markers in primary antiphospholipid syndrome

The pathogenic mechanism underlying the prothrombotic tendency of Hughes' o r antiphospholipid syndrome (APS) has not been elucida;ed. Numerous procoag ulant mechanisms have been tested including platelet activation, monocyte t issue factor (TF) expression and endothelial cell (EC) activation. There is some evidence for the latter from studies on cultured human umbilical vein endothelial cells (HUVEC).:Incubation with antiphospholipid antibodies (aP L) induces EC activation in vitro. We investigated whether there was eviden ce of EC perturbation iii vivo using enzyme-linked immunosorbant assays (EL ISAs) for soluble markers of EC dysfunction. Serum and plasma were collecte d from controls and patients with primary APS and ELISAs performed to quant ify soluble vascular cell adhesion molecule (sVCAM), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6), endothelin-l (ET-I), v on Willebrand factor (VWF) and soluble tissue factor (sTF). in addition, so luble p-selectin (p-selectin) and vascular endothelial growth factor (VEGF) were measured: the former as a marker of platelet activation,the latter as a potential mediator:of TF expression. No significant differences in the l evels of blood-borne soluble markers were detected between the patient and control groups except for VEGF and sTF: patients having significantly highe r levels of VEGF and sTF than controls (p <0.05). These results suggest pla sma soluble tissue factor and VEGF may play a role in the pathogenesis of t hrombosis in APS, although the cell of origin of these molecules remains un clear.