Novel insights into the development of portal vein thrombosis in cirrhosis patients

Abstract

The prognostic impact of portal vein thrombosis (PVT) in liver cirrhosis remains controversial among studies, primarily because the risk stratification of PVT is often lacking. A definition of clinically significant PVT should be proposed and actively improved. Moreover, the risk factors for the development of PVT in liver cirrhosis should be fully recognized to screen and identify high-risk patients. Currently, well-recognized risk factors include a reduced portal vein flow velocity, a worse liver function, splenectomy, liver transplantation, and factor V Leiden and prothrombin G20210A mutations. Novel risk factors include an increased flow volume of portosystemic collateral vessel, thrombopoietin receptor agnonists, and non-selective beta-blockers. In contrast to the traditional perspectives, the abnormalities of procoagulant and anticoagulant factors may not contribute to the development of PVT in liver cirrhosis. Further studies should explore the role of other risk factors, such as antiphospholipid antibodies, methylenetetrahydrofolate reductase C677T gene mutation, hyperhomocysteinemia, and myeloproliferative neoplasms.

Keywords:

• etiology
• liver cirrhosis
• portal vein thrombosis
• prognosis
• risk factor

Financial & competing interests disclosure

X. Qi has received funding from the 2015 Natural Science Foundation of Liaoning Province. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Key issues

• Not all portal vein thrombosis (PVT) events negatively influence the outcomes of liver cirrhosis. Clinically significant PVT should be identified.

• Cirrhotic patients with a portal vein flow velocity of <15 cm/s, the largest collateral vessel’s flow volume >398 ml/min, and worsened liver function are at a high risk of developing PVT.

• Splenectomy and devascularization, liver transplantation, and endoscopic sclerotherapy increase the risk of PVT in liver cirrhosis.

• Thrombopoietin receptor agonists and non-selective beta-blockers induce the development of PVT in liver cirrhosis.

• Abnormalities of procoagulant and anticoagulant factors may not contribute to the development of PVT in liver cirrhosis.

Notes