Hemostasis in liver disease

Abstract

Patients with liver disease have a wide range of coagulation problems. Patients with parenchymal liver disease are likely to have reduced synthesis of proteins and inhibitors (Table 1), whereas dysfibrinogenemia and hyperplenism develop in cirrhosis. Patients with cholestasis without cirrhosis often have elevated levels of fibrinogen, Factors V and VIII, probably due to reduced clearance of proteins (Table 1). The hemostatic defects in liver disease are complex and multifactorial. They are often unpredictable and the mechanisms elusive. Developments in molecular genetics and immunology have shown that both qualitative and quantitative abnormalities of coagulation proteins and protein inhibitors contribute to the abnormalities in liver disease. Future research will certainly result in a better understanding of these defects and more effective therapy.