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.
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)
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
Patients with cirrhosis, regardless of the underlying cause, undergoing TIPS placement, regardless of the indication.
Cohort
Prospective
Not listed
Area Under the Curve (AUC) of primary hemostasis assessed by T-TAS®01 at 10 minutes
The primary outcome measure is the area under the curve (AUC) obtained at 10 minutes of perfusion during the assessment of primary hemostasis using the T-TAS®01 microfluidic system. Measurements are performed with PL chips coated with collagen. Under these conditions, thrombus formation is dependent on von Willebrand factor, allowing evaluation of primary hemostasis at the systemic and portal levels in patients with cirrhosis.
Time to reach 10 kPa above baseline pressure in the T-TAS®01 system
Time required to reach a pressure of 10 kPa above baseline during perfusion in the T-TAS®01 microfluidic system, measured on systemic and portal blood samples
Time to reach 60 kPa above baseline pressure in the T-TAS®01 system
Time required to reach a pressure of 60 kPa above baseline during perfusion in the T-TAS®01 microfluidic system, measured on systemic and portal blood samples
Conventional coagulation parameters at systemic and portal levels
Prothrombin time, activated partial thromboplastin time ratio, factor V, fibrinogen (Clauss method), antithrombin, factor VIII, von Willebrand factor antigen and activity, and ADAMTS-13 activity measured in systemic and portal blood samples
Fibrinolysis parameters at systemic and portal levels
Tissue plasminogen activator antigen and activity, plasminogen activator inhibitor-1 antigen and activity, D-dimers, protease nexin-1, and global fibrinolytic capacity measured in systemic and portal blood samples
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