Hémostase et cirrhose

The liver has an important role to maintain the haemostatic balance. Impaired liver function impacts all stages of hemostasis : primary hemostasis, coagulation and fibrinolysis. Indeed, liver synthesizes almost all procoagulant factors, anticoagulant molecules and proteins involved in the process of fibrinolysis. Its action of removing these molecules is equally important. Liver disease such as cirrhosis may have potentially serious hemostatic effects. Cirrhosis causes impairment of liver tissue that induces a change in the rate of the different actors of hemostasis. However, this leads to a state of unstable balance. Cirrhotic patients have long been considered naturally «self- anticoagulated « because of lower rates of procoagulant factors and elongation conventional coagulation tests such as prothrombin time (PT) or partial thromboplastin time with activator (TCA). However, epidemiological data show that patients with cirrhosis are equally exposed to thrombotic and hemorrhagic complications. While conventional coagulation tests have an interest to explore the degree of liver failure in cirrhotic patients, they are unable to assess concommitantes change of procoagulant and anticoagulant factors. These tests do not reflect the true potential hemostatic of cirrhotic patients and fail to detect patients with an imbalance of coagulation. Global tests such as Thrombinography seem to approach the phenomenon of blood coagulation in vivo through a prolonged time measurement and taking into account the action of anticoagulant molecules measured. This test highlights in cirrhotic patients with a hypercoagulable phenotype.