VWF and hypersplenism: Furthermore, despite a reduction in platelet count or function (due to hypersplenism secondary to portal hypertension, reduced synthesis of thrombopoietin by the liver, bone marrow suppression, increased endothelial production of nitric oxide and prostacyclin, and uraemia), platelet activity is often increased in liver disease as von Willebrand Factor (vWF), a platelet adhesive protein produced in endothelial cells, is often elevated and ADAMTS-13, a vWF-cleaving protease produced by the liver, is often decreased.