BACKGROUND: Hemostatic changes in liver disease are complicated. An overall evaluation of the main hemostatic parameters in patients with different degrees of cirrhosis of the liver has not been reported in Taiwan. METHODS: A series of hemostatic tests and parameters including activated partial thromboplastin time, prothrombin time, thrombin time, bleeding time, factor VIII assay, antithrombin activity, fibrinogen, plasminogen, protamine sulfate test, fibrin(ogen) degradation products, D-dimer, thrombin-antithrombin complex (measured by modified antithrombin), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1, euglobulin lysis test and venous occlusion test were performed in 51 patients with cirrhosis of the liver and 33 healthy controls. Among the cirrhotics, 18 were classified as Child-Pugh group A, 16 were B and 17 were C. RESULTS: Plasminogen, antithrombin and platelet count decreased progressively, starting with group A, then B and then C, relative to the controls. Factor VIII, activated partial thromboplastin time, prothrombin time, bleeding time, D-dimer and fibrin(ogen) degradation products increased progressively starting with group A, to B and then C, relative to controls. Severity of cirrhosis correlated with hemostatic changes. No significant change in the fibrinolytic response after challenge with the venous occlusion test was found in either Child-Pugh groups A, B, C or the controls, though progressive increases in tPA were found starting with group A, to B and then C, relative to controls. CONCLUSIONS: Our study proved a close relationship between the severity of cirrhosis and hemostatic changes. Activated partial thromboplastin time was better than bleeding time or thrombin time to demonstrate the severity of liver damage and hemostatic change in cirrhosis. Because the deterioration of coagulation function and increased fibrinolytic activity paralleled the severity of liver cirrhosis, adequate treatment for cirrhotic bleeding should not only correct the coagulation defects, but should also lower the increasing fibrinolytic activity.
BACKGROUND: Hemostatic changes in liver disease are complicated. An overall evaluation of the main hemostatic parameters in patients with different degrees of cirrhosis of the liver has not been reported in Taiwan. METHODS: A series of hemostatic tests and parameters including activated partial thromboplastin time, prothrombin time, thrombin time, bleeding time, factor VIII assay, antithrombin activity, fibrinogen, plasminogen, protamine sulfate test, fibrin(ogen) degradation products, D-dimer, thrombin-antithrombin complex (measured by modified antithrombin), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1, euglobulin lysis test and venous occlusion test were performed in 51 patients with cirrhosis of the liver and 33 healthy controls. Among the cirrhotics, 18 were classified as Child-Pugh group A, 16 were B and 17 were C. RESULTS: Plasminogen, antithrombin and platelet count decreased progressively, starting with group A, then B and then C, relative to the controls. Factor VIII, activated partial thromboplastin time, prothrombin time, bleeding time, D-dimer and fibrin(ogen) degradation products increased progressively starting with group A, to B and then C, relative to controls. Severity of cirrhosis correlated with hemostatic changes. No significant change in the fibrinolytic response after challenge with the venous occlusion test was found in either Child-Pugh groups A, B, C or the controls, though progressive increases in tPA were found starting with group A, to B and then C, relative to controls. CONCLUSIONS: Our study proved a close relationship between the severity of cirrhosis and hemostatic changes. Activated partial thromboplastin time was better than bleeding time or thrombin time to demonstrate the severity of liver damage and hemostatic change in cirrhosis. Because the deterioration of coagulation function and increased fibrinolytic activity paralleled the severity of liver cirrhosis, adequate treatment for cirrhotic bleeding should not only correct the coagulation defects, but should also lower the increasing fibrinolytic activity.