Hypertension Clinical Trials

Portal vein thrombosis is defined as non-tumoural obstruction of the portal vein or one of its branches. Its incidence is 0.7 to 2.7 per 100,000 patient-years in the general population, and 4.6 per 100 patient-years in patients with cirrhosis. Histological modificaitions fo the portal vein wall and haemostatic changes have been described in cirrhotic patients. The contribution of these changes, both systemic and local, to the development of portal vein thrombosis is debated. One of the hypotheses put forward on the genesis of portal vein thrombosis is as follows: certain bacterial translocations from the digestive tract, promoted by portal hypertension, contribute to endothelial activation resulting in the release of von Willebrand factor and factor VIII, as well as platelet activation and the coagulation cascade, which is dysregulated by cirrhosis and underlying changes in haemostatic balance. Inflammatory phenomena and NETosis may also be involved. Studies suggest that cirrhotic patients have lesions of the glycocalyx located in the portal area, which may be involved in the development of portal vein thrombosis. Patients with cirrhosis may benefit from the placement of a transjugular intrahepatic portosystemic shunt (TIPS). During the TIPS placement procedure, blood is drawn from the internal jugular vein and the portal vein, allowing for parallel biological analyses. The assumption of this study is that haemostasis and inflammation are disrupted differently at the systemic and portal levels in cirrhotic patients.