Abstract:
Portal vein thrombosis (PVT) is one of the most common complications of liver cirrhosis. Its formation increases the mortality of patients with liver cirrhosis and affects the smooth implementation of liver transplantation and postoperative prognosis. Hypercoagulable state is a special mechanism of PVT in patients with liver cirrhosis. In recent years, the multi-dimensional mechanism of PVT has been gradually revealed, and the occurrence of systemic and local inflammatory reactions has damaged the function of vascular endothelial cells and promoted the activation of coagulation system. Abnormal activation of monocyte-macrophage system aggravates local inflammation, enhances platelet adhesion and aggregation, and promotes thrombosis. The imbalance of coagulation and fibrinolysis system leads to a continuous hypercoagulable state ; intestinal dysbacteriosis amplifies inflammation and metabolic disorders, increasing the risk of PVT. By reviewing the latest research progress of the above key mechanisms and their interactions, this paper provides a new perspective for further revealing the molecular and cellular mechanisms of PVT, and points out the future direction for the early diagnosis of PVT and the exploration of new intervention strategies.