Patients with liver cirrhosis have a wide spectrum of abnormalities. Except for factor VIII:C and von Willebrand factor , all procoagulant and inhibitory factors are decrease which is a reflection of impaired protein synthesis. Abnormal fibrinogen and prothrombin molecules can be identified.
Coagulation studies were carried out on patients with chronic liver disease. The clotting defect was complex and involved factors V, VII, IX (Christmas factor ),.
The liver plays a role in the production of clotting factors , as well as red blood cell production. Some of the proteins synthesized by the liver include coagulation factors I (fibrinogen), II (prothrombin), V, VII, VIII, IX, X, XI, XIII, as well as protein C, protein S and antithrombin. Liver parenchymal cells produce all of the coagulation factors involved in the generation of a fibrin clot except for FVIII, which is primarily synthesized by the hepatic endothelium and extrahepatic endothelial cells. Normal coagulation has classically been conceptualized as a Y-shaped pathway, with distinct “intrinsic” and “extrinsic” components initiated by factor XII or factor. Hepatocellular damage in patients with severe liver disease can lead to abnormalities in the production and function of coagulation and fibri- nolytic factors.