Various mechanisms have been postulated for thrombosis in UC which include hypercoagulation (elevated FVIII, fibrinogen, decrease in antithrombin, protein S and protein C), hypofibrinolysis [elevated PAI-1 and lipoprotein (a)], platelet abnormalities, endothelial dysfunction (increased von Willebrand factor), and immunological abnormalities (antiphosphlipid antibodies) [9]. Here, VWF is linked to endothelial dysfunction.