Occlusive portal vein thrombosis as a new marker of decompensated cirrhosis.

Natural history of liver cirrhosis is divided into compensated and decompensated stage. Traditionally, the markers of decompensated cirrhosis include ascites, variceal hemorrhage, hepatic encephalopathy and jaundice. The clinical importance of portal vein thrombosis (PVT) is increasingly recognized in patients with liver cirrhosis. The presence of PVT is not only an independent predictor of failure to control active variceal bleeding and prevent variceal rebleeding, but also significantly associated with increased mortality in patients with liver cirrhosis. Besides, it greatly influences the technical success and outcome of endovascular interventional treatment and liver transplantation for liver cirrhosis and its secondary portal hypertension. Thus, we hypothesize that PVT should be regarded as a critical marker of decompensated cirrhosis, whether clinical events such as the development of ascites, encephalopathy, and variceal bleeding occur or not. Our hypothesis adds PVT into the definition of decompensated cirrhosis and reminds clinicians and investigators that PVT plays a vital role in natural history of liver cirrhosis. Further, it is essential to construct a new system of preventing and treating liver cirrhosis in the presence of PVT.