Published online Dec 18, 2015. doi: 10.4254/wjh.v7.i29.2906
Peer-review started: July 9, 2015
First decision: August 25, 2015
Revised: November 8, 2015
Accepted: December 1, 2015
Article in press: December 2, 2015
Published online: December 18, 2015
Portal vein thrombosis (PVT) is a frequent complication in cirrhosis, particularly in advanced stages of the disease. As for general venous thromboembolism, risk factors for PVT are slow blood flow, vessel wall damage and hypercoagulability, all features of advanced cirrhosis. Actually, the old dogma of a hemorrhagic tendency in cirrhosis has been challenged by new laboratory tools and the clinical evidence that venous thrombosis also occurs in cirrhosis. The impaired hepatic synthesis of both pro- and anticoagulants leads to a rebalanced hemostasis, more liable to be tipped towards thrombosis or even bleeding. Conventional anticoagulant drugs (low molecular weight heparin or vitamin K antagonists) may be used in cirrhosis patients with PVT, particularly in those eligible for liver transplantation, to prevent thrombosis progression thus permitting/facilitating liver transplant. However, several doubts exist on the level of anticoagulation achieved as estimated by coagulation tests, on the efficacy of treatment monitoring and on the correct timing for discontinuation in non-transplant candidates, while in transplant candidates there is expert consensus on continuing anticoagulation until transplantation. The recent introduction of direct acting oral anticoagulant drugs (DOACs) in other clinical settings generates much interest on their possible application in patients with cirrhosis and PVT. However, DOACs were not evaluated yet in patients with liver disease and cannot be recommended for the present time.
Core tip: Impaired liver synthesis of both pro- and anticoagulants maintains a haemostatic balance in advanced liver disease, but this balance is more unstable than in healthy subjects and can be easily tipped towards thrombosis or bleeding. Portal vein thrombosis (PVT) frequently occurs in advanced stages of cirrhosis and, if occlusive or extensive, may complicate or impede liver transplant. Therefore, prevention and treatment of PVT are frequent issues in cirrhosis patients, particularly in those eligible to liver transplant. Current treatments are with low molecular weight heparin or vitamin K antagonists and should be continued until transplantation in liver candidates, whereas no consensus exists regarding the duration of anticoagulation in non-transplant candidates.