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.

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. Portal vein thrombosis associated with cirrhosis, which is most often non-occlusive (70%), is characterised by histological changes in the portal vein wall and the presence of an intraluminal thrombus.

In cirrhotic patients, histological changes are described at the portal level. In response to portal hypertension, the calibre of the portal vein, where circulation is at low pressure and high compliance, increases. In response to this mechanical stress, intimal hypertrophy and fibroblast proliferation are observed. In cases of portal vein thrombosis, these changes are more pronounced. Changes in haemostatic balance are also observed in these patients. Thrombocytopenia and decreased synthesis of coagulation factors on the one hand, and decreased coagulation cascade and fibrinolytic regulatory factors on the other, contribute to creating a new fragile haemostatic balance. 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 (VWF) and factor VIII, as well as platelet activation and the coagulation cascade, which is dysregulated by cirrhosis and underlying changes in haemostatic balance.

This hypothesis is supported by several studies showing that cirrhotic patients have higher portal than systemic levels of VWF, factor VIII and lipopolysaccharides. Inflammatory phenomena and NETosis may also be involved.

The vascular endothelial surface is covered by the glycocalyx, with antithrombotic and anti-inflammatory effects that regulates vascular permeability. The endothelial glycocalyx has three major components: proteoglycans binding to the endothelial membrane, sulphated glycosaminoglycans bound laterally to proteoglycans, and plasma proteins. 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. To our knowledge, studies conducted to date have not investigated haemostasis under flow conditions, which are more physiological than static investigations.

Inclusion Criteria:

• Adult patients (aged ≥18 years) covered by a social security scheme or entitled beneficiaries
• Patients followed for a cirrhotic condition at Paul Brousse Hospital and undergoing placement of a TIPS (transjugular intrahepatic portosystemic shunt)

Exclusion Criteria:

• Patient unwilling to participate in the study
• Patient with a contraindication to TIPS placement
• Patient with a known hemostatic disorder unrelated to cirrhosis
• Patient receiving treatment that interferes with hemostasis and has not been discontinued for the procedure
• Patient receiving systemic corticosteroid therapy
• Patient under legal protection
• Patient not covered by a social security scheme

Patients with cirrhosis, regardless of the underlying cause, undergoing TIPS placement, regardless of the indication.