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BACKGROUND AND AIM: The development of acute pancreatitis (AP) is strongly linked to blood clotting and fibrinolysis issues. Modern clinical practices now utilize advanced blood markers like thrombin-antithrombin III complex (TAT), plasmin-α2-plasmin inhibitor complex, thrombomodulin (TM), and tissue plasminogen activator-inhibitor complex (t-PAIC) to assess thrombosis risk. Our study used a highly sensitive chemiluminescence technique to measure these markers in AP patients, aiming to determine their early predictive value for AP severity. METHODS: There were 173 patients with AP, all of whom developed symptoms within 72 h; 102 individuals had onset symptoms within 48 h. The biomarkers were measured upon admission before determining the severity of AP. RESULTS: The levels of TAT, plasmin-α2-plasmin inhibitor complex, TM, and t-PAIC were significantly higher in the severe acute pancreatitis (SAP) group compared with the mild acute pancreatitis and moderate severe acute pancreatitis groups. For the patients within 72 h of onset, TAT, TM, and t-PAIC predicted the occurrence of SAP. For the patients within 48 h of onset, TAT and t-PAIC predicted the occurrence of SAP. The area under the curve (AUC) of prediction models is similar to Bedside Index for Severity in Acute Pancreatitis (BISAP) but significantly higher than C-reactive protein (P < 0.05). Notably, t-PAIC had a larger AUC than TAT, BISAP, and C-reactive protein. CONCLUSION: In the initial 48 h, plasma TAT and t-PAIC levels may predict the development of SAP. Within 72 h, plasma levels of TAT, TM, and t-PAIC may predict the development of SAP, and the TAT + TM + t-PAIC prediction model achieved a maximum AUC of 0.915, comparable to BISAP.

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Background/Objectives: The coagulation cascade due to tissue damage is considered to be one of the causes of poor prognostic outcomes in patients with acute exacerbations of interstitial lung disease (AE-ILD). This study aimed to confirm coagulopathy in AE-ILD by evaluating the differences in the clinical characteristics of coagulation/fibrinolysis markers between stable ILD and AE-ILD. Methods: Overall, 81 patients were enrolled in this retrospective study and categorized into the following two groups: a chronic ILD group comprising 63 outpatients and an acute ILD group comprising 18 inpatients diagnosed with AE-ILD. Serum markers, including thrombin-antithrombin III complex (TAT), D-dimer, plasmin-α2 plasmin inhibitor complex (PIC), and surfactant protein D (SP-D), were compared between the groups. Results: Among the 18 patients with acute ILD, 17 did not meet the International Society of Thrombosis and Hemostasis scoring system for disseminated intravascular coagulation. In acute ILD, the SP-D levels were statistically significantly positively correlated with TAT, D-dimer, and PIC levels, while the Krebs von den Lungen 6 (KL-6) levels showed no correlation with any of these coagulation/fibrinolytic markers. A positive correlation was observed between SP-D levels and TAT, D-dimer, and PIC levels in acute ILD. Serum TAT, D-dimer, and PIC all showed good area under the receiver operating characteristic (ROC) curve (AUC) values in ROC analysis for the diagnosis of acute ILD. Conclusions: In the clinical setting of AE-ILD, it may be important to focus not only on alveolar damage markers such as SP-D but also on coagulation/fibrinolytic markers including TAT, D-dimer, and PIC.

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BACKGROUND: Coagulation and fibrinolysis are distinct processes that are highly correlated. Cells control coagulation and fibrinolysis by expression of tissue factor and urokinase-type plasminogen activator receptor on their surface. Tumor cells express these proteins, adjust their microenvironment and induce tumor exacerbation. We hypothesized that the expression of plasma markers for coagulation and fibrinolysis in patients with soft tissue sarcomas (STSs) was dependent on the level of tumor malignancy. To elucidate which markers are predictive of recurrence, metastasis and prognosis, coagulation or fibrinolysis, we analyzed the correlation between plasma levels of thrombin-antithrombin III complex (TAT), soluble fibrin (SF), plasmin-α2 plasmin inhibitor complex (PIC), D-dimer (DD) and clinical parameters in patients with STSs. METHODS: TAT, SF, PIC or DD were measured in pre-treatment blood samples from 64 patients with primary STSs and analyzed with clinicopathological parameters, and 5-year recurrence free survival (RFS), 5-year metastasis free survival (MFS) and 5-year overall survival (OS) were evaluated. RESULTS: The metastasis group had significantly higher DD (p = 0.0394), PIC (p = 0.00532) and SF (p = 0.00249) concentrations than the group without metastasis. The group that died of disease showed significantly higher DD (p = 0.00105), PIC (p = 0.000542), SF (p = 0.000126) and TAT (p = 0.0373) than surviving patients. By dividing the patients into low and high groups, the group with high DD, PIC, SF and TAT showed significantly lower 5-year MFS and 5-year OS than the corresponding low group. Furthermore, in multivariate COX proportional hazard analysis of continuous variables for 5-year MFS, only PIC was found to be a significant factor (HR: 2.14). CONCLUSION: Fibrinolysis was better than coagulation at reflecting the disease condition of patients with STS. Notably, PIC levels ≥ 1.1 can not only predict the risk of metastasis and poor prognosis, but also increasing PIC levels correspond to further increases in risks of metastasis and poor prognosis.

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BACKGROUND: The intimate relationship between coagulation and fibrinolysis in malignant tumors is a well-known phenomena, with the malignant phenotype enhancing coagulation and fibrinolysis. We hypothesized that soft tissue sarcoma (STS) affects the expression of coagulation and fibrinolysis markers, which could be used to distinguish STS from benign soft tissue tumors. We analyzed the correlations between plasma levels of D-dimer (DD), plasmin-α2 plasmin inhibitor complex (PIC), soluble fibrin (SF), and thrombin-antithrombin III complex (TAT) in benign soft tissue tumors and STS to elucidate whether these markers can be used to predict STS. METHODS: Plasma DD, PIC, SF and TAT levels in primary soft tissue tumors (benign 67, STS 68) were measured before biopsy or treatment. The marker levels were analyzed and compared to various clinicopathological parameters. RESULTS: In malignancy (STS), the average DD, PIC and SF levels were significantly higher than in benign tumors. Multivariate logistic analysis of continuous variables indicated that only PIC exhibited a significant difference (OR: 24.5, 95%CI: 3.55-170, p = 0.0012). Receiver operating characteristic curve analysis produced area under the curve values for DD: 0.691, PIC: 0.784, SF: 0.734 and TAT: 0.588. Youden's index was used to establish thresholds of 0.37 (DD), 0.80 (PIC), 0.90 (SF) and 0.82 (TAT). Threshold values for PIC and SF indicated high specificity (0.881, 0.791) and high positive predictive value (0.818, 0.745), respectively. The highest accuracy value among the markers was observed for PIC (0.704). Significant differences in multivariate analysis of binary variables were demonstrated by categorizing low and high groups based on their threshold, PIC (≥0.80) (OR: 3.36, 95%CI: 1.19-9.43, p = 0.0212) and SF (≥0.90) (OR: 2.63, 95%CI: 1.04-6.66, p = 0.0404) . CONCLUSIONS: Of the coagulation and fibrinolysis markers studied, increased PIC levels were related to STS and over 0.80 PIC was the most suitable for the prediction of STS, which, along with other diagnostic tools, represents a helpful subsidiary tool for the prediction of STS.

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PURPOSE: Portal vein thrombosis (PVT) following hepatectomy is potentially life-threatening. We aimed to evaluate the incidence of PVT after hepatectomy for hepatocellular carcinoma and identify coagulation and fibrinolytic factors that could predict early-stage postoperative PVT. METHODS: A retrospective analysis was conducted on 65 hepatocellular carcinoma patients who underwent radical hepatectomy. The risk factors for postoperative PVT were identified based on univariate and multivariate analyses, and the levels of coagulation and fibrinolytic factors were measured during the perioperative period. RESULTS: The incidence of PVT after hepatectomy was 20.0%. The patients were divided into two groups: those with PVT (n=13; PVT group) and those without PVT (n=52; no-PVT group). The frequency of the use of the Pringle maneuver during surgery was higher in the PVT group than in the no-PVT group, and the postoperative/preoperative ratios of thrombin-antithrombin III complex (TAT) and of D-dimer were significantly higher in the PVT group. CONCLUSION: A high incidence of PVT was found in hepatocellular carcinoma patients after hepatectomy. The frequency of the Pringle maneuver is a potential risk factor for postoperative PVT, and the postoperative/preoperative TAT and D-dimer ratios may be used as early predictors of PVT after hepatectomy for hepatocellular carcinoma.

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BACKGROUND: Venous thromboembolism (VTE) is an important complication in patients with malignant tumors. Its exact diagnosis and treatment are still lacking. We used a high-sensitive chemiluminescence method to detect thrombin-antithrombin III complex (TAT), plasmin-α2-plasmininhibitor complex (PIC), thrombomodulin (TM), and tissue plasminogen activator-inhibitor complex(t-PAIC) in combination with D-dimer and fibrin degradation product (FDP) to analyze their diagnostic and prognostic value in patients with malignant tumors. METHODS: In total, 870 patients with confirmed malignant tumors were included, 82 of whom had diagnosed VTE; 200 healthy individuals were classified as the control group. The TAT, PIC, TM, and t-PAIC were detected using Sysmex HISCL5000 automated analyzers, whereas FDP and D-dimer were detected using Sysmex CS5100 coagulation analyzer. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic efficiency. Survival probabilities were determined using Kaplan-Meier analysis, and multivariate analyses were performed using a Cox regression model. RESULTS: Compared with healthy controls, patients with malignant tumors showed significantly elevated TAT, PIC, TM, t-PAIC, D-dimer, and FDP. Similarly, compared with patients in the non-thrombosis group, those in the thrombosis group showed significantly elevated levels of the above mentioned markers. Logistic regression analysis showed that TAT, PIC, TM, t-PAIC, D-Dimer, and FDP were all associated with VTE. ROC analysis showed that "TAT+PIC+TM+t-PAIC+D-dimer+FDP"showed the highest sensitivity and specificity. Patients with elevated TAT, PIC, TM, and t-PAIC had a significantly shorter survival. Multivariate Cox survival analysis showed that TM and t-PAIC were significantly associated with poor prognosis. In addition, the incidence of VTE was significantly lower in patients with malignant tumors who were treated with low-molecular-weight heparin (LMWH), and their survival period was significantly longer than that of patients with malignant tumors who were not treated with LMWH. CONCLUSION: TAT, PIC, TM, and t-PAIC combined with D-dimer and FDP were better than the application of a single marker in the diagnosis of VTE in patients with malignant tumors. TAT and PIC can be used as sensitive markers in the diagnosis of VTE but not as prognostic markers. TM and t-PAIC might be independent prognostic indicators in patients with malignant tumors, regardless of the state of thrombus.

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PURPOSE: Patients with fractures of the pelvis and/or lower extremities are at a high risk of developing postoperative venous thromboembolism (VTE). The purpose of this study was to determine whether the thrombin-antithrombin III complex (TAT) tests could be used for postoperative screening of VTE in patients with lower limb or pelvic fractures. METHODS: We enrolled 133 patients who underwent surgical treatment for fracture of the pelvis or lower extremities. TAT and D-dimer levels were compared in patients with and without VTE. Receiver operating characteristic (ROC) curve analysis was done and the appropriate TAT and D-dimer cutoff levels were determined for VTE screening. RESULTS: VTE was diagnosed in 41 patients (30.8%). Patients with VTE had significantly higher levels of TAT and D-dimer on postoperative days 1, 3, and 7 than those without VTE, respectively. ROC curve analysis suggested that TAT test at postoperative day 7 had the highest accuracy for predicting postoperative VTE. With the optimal cutoff TAT level of 3.0 ng/mL, sensitivity and specificity were 93.3% and 70.1%, respectively. With the optimal cutoff D-dimer level of 7.4 µg/mL, sensitivity and specificity were 93.3% and 57.0%, respectively. CONCLUSION: TAT levels measured at postoperative day 7 could be the most useful parameter for screening postoperative VTE. TAT can be used as a screening tool for screening postoperative VTE in patients with lower limb and pelvic fractures.

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Case: A healthy 40-year-old man was admitted with severe coagulopathy that developed after Rhabdophis tigrinus bites. On admission, he showed significantly elevated levels of thrombin-antithrombin III complex (60 ng/mL), plasmin-alpha 2-plasmin inhibitor complex (22.3 µg/mL), and fibrinogen degradation products (592 µg/mL). He subsequently developed severe hypofibrinogenemia (50 mg/dL). Outcome: Antivenom was given 28 h after the patient was bitten, following which his hemorrhagic symptoms resolved. By day 3 of admission, scabs had formed over the bite wounds. Furthermore, his fibrinogen levels increased to >100 mg/dL, while his thrombin-antithrombin III complex, plasmin-alpha 2-plasmin inhibitor complex, and fibrinogen degradation product levels normalized. He was discharged on day 6 of admission. Conclusion: Rhabdophis tigrinus bites induced disseminated intravascular coagulation with a fibrinolytic phenotype, which completely recovered with antivenom treatment.

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The risk of bleeding is a well-known complication in patients on hemodialysis (HD). The aim of this prospective study was to determine the lowest single bolus dose of low-molecular-weight heparin nadroparin for safe and effective HD in patients with a bleeding risk. Forty HD patients were divided into 4 subgroups with 10 participants (diabetics with and without a bleeding risk, nondiabetics with and without a bleeding risk). The actual starting bolus dose was decreased by 25% after the initial 4 weeks, further decreased by 25% of the starting dose after 4 weeks, and changed due to extracorporeal circuit clotting in the last 4 weeks. The parameters of coagulation were measured at the beginning, after 2 and 4 h of HD sessions. A significant reduction of nadroparin (first vs. last HD session) was observed in: diabetics with a bleeding risk (49.66 ± 12.33 vs. 28.78 ± 9.60 IU/kg/HD; P<0.001), diabetics without a bleeding risk (50.70 ± 15.23 vs. 33.95 ± 16.97 IU/kg/HD; P<0.001), and nondiabetics with a bleeding risk (61.25 ± 18.68 vs. 32.96 ± 10.06 IU/kg/HD; P<0.001). Altogether, the reduction of the nadroparin dose in these groups was 42.05%; 33.04%, and 46.19%, respectively. Although anti-Xa at hour 4 at the end of the study was <0.4 IU/mL in our diabetic and nondiabetic patients without a risk of bleeding, serious clottings in the extracorporeal circuit and vascular access thromboses were not found. This study demonstrated for the first time that individually optimized doses of nadroparin are sufficient for safe and effective HD in patients with a bleeding risk.

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@# ObjectiveTo determine the change of coagulation in acute brain infarction.MethodsBlood samples were taken intravenously from 57 patients with acute brain infarctions (within 24hr) and the thrombin time(TT), prothrombin time(PT), activated partial thromboplastin time(APTT), fibrinogen(FIB) levels were detected serially at the time of instant admission, 1st day ,3rd day and 7th day after routine therapy, including 21 patients whose thrombin antithrombin III complex(TAT) levels were detected at the same time.ResultsTAT levels were significant increased in acute brain infarctions, especially in acute progress stroke, but TT, PT, APTT were not significantly different before and after routine treatment. FIB levels were higher at 7th day than pre-treatment. ConclusionTAT levels can be served as a marker of progress stroke.

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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.

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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.

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BACKGROUND: The purpose of this study is to evaluate the diagnostic usefulness of the quantitation of D-dimer, thrombin-antithrombin III complex (TAT) and prothrombin fragment 1 2 (F1 2) in patients with DIC or venous thrombosis. METHODS: The quantitation of D-dimer, TAT and F1 2 by ELISA (Behring, Germany) were done with the specimens from eighty eight patient plasma. The patients were classified as DIC, probable DIC and non-DIC based on the DIC criteria by reserach committee in Japan, and the patients with deep vein thrombosis (DVT) or pulmonary embolism (PE) were included. RESULTS: All eighteen DIC patients showed the increased D-dimer ELISA and fourteen patients showed the increased TAT and F1 2. According to the results of quantitative D-dimer, TAT and F1 2 tests, probable DIC and the group with increased results of above three tests among non-DIC were considered as DIC. Two patients with PE showed increased results of above three tests. Among nine DVT patients, eight patients showed increased results of D-dimer ELISA and F1 2, but TAT was increased in only six patients. Among forty six patients with negative results of D-dimer semiquantitation (latex agglutination), twenty seven patients (59%) revealed increased results of D-dimer quantitation (ELISA). CONCLUSIONS: D-dimer quantitation by ELISA is the most sensitive test in the diagnosis of DIC and venous thrombosis. The quantitation of D-dimer, TAT and F1 2 can increase the diagnostic rate of DIC and venous thrombosis, and the developement of the new quatitating reagents with more rapid and individual procedures will contribute to the accurate and rapid diagnoses of them.

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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.

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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.

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