Published online Sep 28, 2012. doi: 10.3748/wjg.v18.i36.5014
Revised: April 17, 2012
Accepted: April 20, 2012
Published online: September 28, 2012
Portal vein thrombosis (PVT) is one of the most common complications occurring during the natural course of liver cirrhosis. Even though PVT is often asymptomatic, the worsening of liver function, an unexpected episode of gastrointestinal bleeding or ascitic decompensation may be landmarks of PVT development. Beyond these clinical manifestations, it is debated whether PVT really has an impact on liver cirrhosis natural history or rather represents only one of its consequences. Probably PVT development should not only be considered as a matter of impaired blood flow or pro-coagulation tendency. On one hand, PVT seems a consequence of the worsening in portal vein outflow due to the increased hepatic resistance in cirrhotic livers. On the other hand, vascular microthrombosis secondary to necroinflammation may cause liver ischemia and infarction, with loss of hepatic tissue (parenchymal extinction) which is replaced by fibrotic tissue. Therefore, PVT might also be considered as the overt manifestation of the liver fibrosing process evolution and anticoagulant therapy may thus have microscopic indirect effects also on the progression of liver disease. At present, a connection between PVT development and the progression of liver fibrosis/cirrhosis has not yet been demonstrated. Nevertheless, it is not clear if PVT development may worsen cirrhotic patients’ outcome by itself. Some authors tried to assess liver transplant benefit in PVT cirrhotic patients but data are contrasting. In this review, we will try to answer these questions, providing a critical analysis of data reported in literature.