Summary
The pathogenic mechanism underlying the prothrombotic tendency of Hughes’ or antiphospholipid
syndrome (APS) has not been elucidated. Numerous procoagulant mechanisms have been
tested including platelet activation, monocyte tissue 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
(aPL) induces EC activation in vitro. We investigated whether there was evidence of EC perturbation in vivo using enzyme-linked immunosorbant assays (ELISAs) for soluble markers of EC dysfunction.
Serum and plasma were collected from controls and patients with primary APS and ELISAs
performed to quantify soluble vascular cell adhesion molecule (sVCAM), soluble intercellular
adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6), endothelin-1 (ET-1), von Willebrand
factor (vWF) and soluble tissue factor (sTF). In addition, soluble 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 levels of blood-borne soluble markers were detected between the
patient and control groups except for VEGF and sTF, patients having significantly
higher levels of VEGF and sTF than controls (p <0.05). These results suggest plasma
soluble tissue factor and VEGF may play a role in the pathogenesis of thrombosis in
APS, although the cell of origin of these molecules remains unclear.
Key words
Endothelium - antiphospholipid syndrome