Activation and regulation of hemostasis in acute liver failure and acute pancreatitis

Acute liver failure and acute pancreatitis are accompanied by substantial changes in the hemostatic system. In acute liver failure, defective synthesis of coagulation factors and intravascular activation of coagulation results in thrombocytopenia and reduced levels of proteins involved in coagulation and fibrinolysis. Acute pancreatitis may be accompanied by intravascular activation of hemostasis mediated by inflammation and exposure of pancreatic tissue factor to the bloodstream. In animal models for both diseases, activation of hemostasis appears to contribute to the progression of the disease. Consequently, the use of anticoagulants may, in theory, be beneficial in humans. In practice, however, clinical use of anticoagulants in these patients is likely hampered by a substantial bleeding risk.