Portal vein thrombosis in cirrhotic patients - it is always the small pieces that make the big picture

Abstract

Portal vein thrombosis (PVT) is a frequent and serious complication in patients with liver cirrhosis (LC). Recently, a new classification of PVT was proposed, although the functional component was not completed included. The status of liver disease (compensated/decompensated) should be added to this classification. Reduced portal flow velocity and the acquired hypercoagulable status associated with LC are the main risk factors for PVT development, although endothelial dysfunction may play an important role that needs to be further evaluated. The European Association for the Study of the Liver and the American Association for the Study of Liver Disease recommend that the anticoagulant treatment should be consider in cirrhotic patients with PVT. Low molecular weight heparin and vitamin K antagonists proved their efficacy and relatively safety in PVT treatment, although in addition to recanalization rates, more complex end-points such as mortality and decompensation rate should be evaluated. The new oral anticoagulant therapies offers the advantage of oral administration in the absence of laboratory monitoring, however, there are a few reports regarding their use in cirrhotic patients, most of them referring to compensated isolated cases. Transjugular intrahepatic portosystemic shunt could be an alternative if thrombosis progresses despite anticoagulatant therapy and/or when PVT is associated with portal hypertension complications. The aim of this editorial is to discuss the different aspects of pathophysiology, clinical relevance, diagnosis and management of PVT in patients with LC.

A Preclinical Porcine Model of Portal Vein Thrombosis in Liver Cirrhosis

“…Further, the present literatures do not establish with certainty the role of antithrombotic agents in preventing PVT extension in cirrhosis patients [7].…”

Evaluation of Coagulation, Fibrinolysis and Endothelial Biomarkers in Cirrhotic Patients With or Without Portal Venous Thrombosis

“…There is additional evidence that markers of endothelial dysfunction, including P-selectin, vWF and isoprostanes are upregulated in cirrhotic patients. 27 Both t-PAIC and TM are molecules involved in the endothelial system. 28 Increased t-PAIC and TM can be used to infer endothelial cell injury, 29 which is consistent with elevated FⅧ: c and vWF: Ag, as previously mentioned.…”

Sufficient hepatic artery flow compensates for poor portal vein flow after liver transplantation in patients with portal vein thrombosis

“…Liver cirrhosis (LC) is associated with an increased risk of portal hypertension and portal vein thrombosis (PVT) . The risk of PVT is likely dependent on the combined effects of reduced blood flow in the portal venous system due to liver fibrosis, endothelial dysfunction, and the presence of a pro‐thrombotic state driven by the high factor VIII/protein C ratio that parallels the severity of liver disease . PVT is often encountered in liver transplant (LT) candidates and was previously considered a contraindication to LT because of poor intra‐ and postoperative outcomes .…”