 BACKGROUND AND JUSTIFICATION The occurrence of portal vein thrombosis PVT radically changes the prognosis of cirrhotic patients, particularly those awaiting liver transplantation. If this happens, it occurs in about 8-10 year in patients with cirrhosis awaiting liver transplantation. Some studies have suggested the involvement of various risk factors for the development of PVT in cirrhotic patients, including the classic congenital and acquired thrombophilic conditions 1-6, although contributions of our research group have shown that a key element in the development of PVT in these patients is the decreased velocity of portal blood flow 7, 8. The possible contribution of the von Willebrand factor VWF and ADAMTS-13, produced by the liver stellate cells 9, for the development of PVT is rather poorly documented. In a recent observational study of the proponent 10, conducted on 84 patients with liver cirrhosis, it was found that the level of circulating ADAMTS-13 is significantly lower in the group with PVT median 16.8 vs. 69.1, p 0.0047 and independently associated with the presence of portal thrombosis p 0.007. However, given the non-longitudinal nature of the study, it is possible that the decreased level of ADAMTS-13 observed is the consequence and not the cause of PVT. It is also yet to investigate the association of ADAMTS-13 level with the specific etiology of cirrhosis viral, alcoholic, idiopathic, etc. and the resulting inflammation during the course of the disease. 