The imbalance between coagulation and fibrinolysis is related to the severity of the illness and the prognosis in sepsis

OBJECTIVES: The coagulation and fibrinolytic system appears to be activated by the septic process independently, leading to the syndrome of disseminated intravascular coagulation (DIC). In this study, we investigated the changes within the hemostatic system related to the severity of the illness and the prognosis in patients with sepsis. METHODS: Plasma thrombin-antithrombin III (TAT) and plasmin-alpha 2-antiplasmin (PAP) complexes were measured using ELISA methods in 32 patients with sepsis and 20 controls and were analyzed according to the APACHE III scores and survival of the patients. RESULTS: Plasma TAT and PAP in patients with sepsis were significantly higher than controls. Nonsurvivors showed greater levels of TAT (21.7 +/- 22.3 ng/mL) and lower levels of PAP (628.4 +/- 378.1 ng/mL) than survivors (TAT: 11.1 +/- 11.2 ng/mL; PAP: 857.1 +/- 364.1 ng/mL). The imbalance between coagulation and fibrinolysis described as TAT/PAP ratio was closely related with APACHE III scores in patients with sepsis (r = 0.47) and the TAT/PAP ratio in nonsurvivors was significantly higher compared with survivors (34.4 +/- 21.4 vs. 14.4 +/- 13.8). CONCLUSION: In sepsis, both coagulation and the fibrinolysis system are activated and the imbalance between coagulation and fibrinolysis predisposes to the hypercoagulation state and is closely related to the severity of the disease and the prognosis.

The Changes in Coagulation and Fibrinolytic Activities in Acute Myocardial Infarction Patients Treated with Recombinant Tissue Plasminogen Activator and Urokinase

BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.

The Changes in Coagulation and Fibrinolytic Activities in Acute Myocardial Infarction Patients Treated with Recombinant Tissue Plasminogen Activator and Urokinase

BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.

Alterations of Coagulation and Fibrinolysis System in Lung Cancer / 대한내과학회지

OBJECTIVES: It is well known that malignant diseases exhibit an increased propensity to clotting and fibrinolytic aberrations and early detection of these hemostatic alterations is very important for the rapid institution of appropriate treatment of thromboembolic and hemor rhagic complications in patients with malignant disease. The incidence of these abnormalities in lung cancer was reported from 20% up to 95% according to various investigators using different hemostatic parameters. We measured the concentrations of plasma thrombin antithrombin III complex(TAT) and plasmin-alpha2-plasmin inhibitor complex(PIC), which are newly developed sen sitive molecular markers of coagulation and fibrinolysis system respectively in patients with lung cancer and determined the degree of these hemostatic abnormalities according to the histologic types and different clinical stages in patients with lung cancer. METHODS: We measured the concentrations of plasma TAT and PIC in 62 patients with histologically confirmed lung cancer, and we determined stage radiologically in non-surgical patients and pathologically in surgical pa tients. The plasma TAT and PIC levels were assayed using a solid phase enzyme immunoassay with Enzygnost-TAT kit(Behringwerke, Marburg, Germany) and Enzygnost-PAP kit(Behringwerke, Marburg, Germany), respectively. RESULTS: The concentrations of plasma TAT(6.8+/-4.8 ng/mL) and PIC(644.3+/-330.5 ng/mL) in patients with lung cancer were significantly increased compared to those of plasma TAT(2.8+/-1.2 ng/mL) and PIC(240.4+/- 69.7 ng/mL) in control subjects(p 0.05). CONCLUSIONS: There was a subclinical activation of coagulation and fibrinolysis system in patients with lung cancer although they don't have overt clinical evidences of thromboembolism or hemorrhage. But there were no different activation of coagulation and fibrinolysis system according to histologic types and clinical stages.