Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the impact of blood coagulation and fibrinolysis on the clinical features of eclamptic patients (n = 20) in Bangladesh. The variables used were edema, proteinuria, blood pressure, number of convulsions, level of consciousness at the time of admission, thrombin antithrombin complexes (TAT), antithrombin (AT) III (%) activity and antigen, D dimer fibrin degradation product and alpha 2-plasmin inhibitor-plasmin complex (PIC) in plasma. Canonical correlation analysis was made to obtain clinical index, eclampsia index and two coagulation indices. On admission, the mean values of coagulation parameters were AT III activity: 83.2% (range 57-108), TAT complex: 47.6 ng/ml (range 11.5-60), D dimer: 1,693 ng/ml (range 417-8,276) and PIC 1.4 mg/ml (range 0.4-3.3). We found a significant correlation between the eclampsia index and clinical index (r = 0.601; p = 0.01). Gestosis index, clinical index, and eclampsia index have also a strong correlation with the coagulation index (r = 0.695, p < 0.005; r = 0.871, p < 0.0001 and r = 0.805, p < 0.0001, respectively). Coagulation and fibrinolysis were markedly activated in eclampsia. The correlation between the clinical status and coagulation status in this study suggested a close relation between the coagulation and the development and progression of the disease.
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PMID:Blood coagulation and fibrinolysis in eclamptic patients and their correlation with the clinical signs. 777 98

Plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC) and active plasminogen activator inhibitor (PAI) were assayed in 66 cases of disseminated intravascular coagulation (DIC). Significant elevation of both TAT and PIC was observed in all cases of DIC. Most elevated levels of TAT were seen in DIC with acute promyelocytic leukaemia (APL) and sepsis. The highest levels of PIC were seen in DIC with APL but were much lower in sepsis. A significant elevation in active PAI was observed in DIC due to acute leukaemia (apart from APL), chronic myeloid leukaemia and sepsis, but not in APL, non-Hodgkin lymphoma and cancer. Active PAI was higher in patients with multiple organ failure (MOF) than in those without MOF while PIC was lower in patients with this complication. Thus, the balance of coagulation and fibrinolysis varied according to the underlying cause of DIC; APL had more dominant activation of fibrinolysis, while sepsis had greater activation of coagulation. It is suggested that the inhibition of secondary fibrinolytic activation plays an important role in the progression of MOF by the disturbance of the microcirculation.
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PMID:Study of the balance between coagulation and fibrinolysis in disseminated intravascular coagulation using molecular markers. 786 91

The influence of mitral valve area (MVA) on hemostatic conditions was assessed in patients with rheumatic mitral stenosis (MS) without atrial thrombus who underwent percutaneous mitral valvuloplasty (PMV). The Doppler-derived MVA and hemostatic variables were obtained before and 2-3 months after PMV. Hemostatic tests included measurements of beta-thromboglobulin and platelet factor 4 levels as indexes of platelet activation, fibrinopeptide A and thrombin-antithrombin complex as markers of fibrin generation, and D-dimer and plasmin-alpha 2-plasmin inhibitor complex as indexes of active fibrinolysis. Thirty-three measurements in 17 MS patients were subdivided into three groups: group A, 16 samples when MVA was < 1.5 cm2, group B, 12 samples obtained when MVA was 1.5 - < 2.0 cm2, and group C, 5 samples obtained when MVA was > or = 2.0 cm2. The mean level of beta-thromboglobulin was significantly lower in group C (43.6 +/- 32.4 ng/ml) than in group A (142.5 +/- 132.5 ng/ml) or B (163.8 +/- 179.8 ng/ml) (p < 0.05). The incidence of abnormal beta-thromboglobulin was also significantly lower in group C (20%) than in group A (67%) or B (73%) (p < 0.05). Other mean values or incidence of abnormal values of other hemostatic parameters did not differ between the groups. The hemostatic change induced by PMV was examined in 15 MS patients with no change in cardiac rhythm after PMV therapy. The patients were divided into suboptimal (MVA widening < 0.5 cm2, n = 7) and optimal (> or = 0.5 cm2, n = 8) groups. No favorable hemostatic changes were achieved by PMV in the suboptimal group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relationship of mitral valve area to hemostatic condition in rheumatic mitral stenosis]. 793 73

Selected coagulation and fibrinolytic factors were evaluated in plasma and synovial fluid (SF) of 10 rheumatoid arthritis (RA) patients. Increased levels of fibrinogen were observed in plasma (p < 0.01), but only a trace amount of structurally intact fibrinogen was detected in the SF of RA patients, while immunostaining showed deposits of insoluble fibrin in their synovial membranes. Reduced levels of protein C, antithrombin III and coagulation factors II, V, VII, VIII, IX, XII and XIII (p < 0.01), and high levels of thrombin-antithrombin III (TAT) complexes (p < 0.01), were found in SF as compared to their corresponding plasma levels. The increased levels of fibrinogen, TAT complexes, B beta 15-42 peptide and plasminogen activator inhibitor-1 (PAI-1) in plasma (p < 0.01) are consistent with an enhanced fibrin turnover and endothelial perturbation due to a systemic inflammatory state. Plasminogen and alpha 2-plasmin inhibitor activity in SF were significantly reduced as compared to the plasma levels (p < 0.01), whereas an increase in PAI-1 activity was found in SF as compared to plasma (p < 0.01). The detection of D-dimer and B beta 15-42 peptide (p < 0.01) in SF suggests an involvement of plasmin in the degradation of fibrin generated in synovial tissue. The high levels of elastase-alpha 1-proteinase inhibitor complexes and of thrombin-increasable fibrinopeptide A, as well as the pattern of fibrinogen degradation as identified in SF by double-dimension immunoelectrophoresis, suggest that elastase released from exudated granulocytes may play an important role in fibrino(geno)lysis and tissue damage in RA joints.
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PMID:Elastase- and plasmin-mediated fibrinolysis in rheumatoid arthritis. 796 May 5

Eighty-four patients were examined for blood coagulability during the acute phase of Bell's palsy. Abnormally high levels of thrombin-antithrombin III complex (TAT) and alpha-2 plasmin inhibitor-plasmin complex (PIC) were found, with these increases statistically significant. Values tended to be higher in patients within 3 days after occurrence of the palsy when compared to values in patients 4 days or more later. Abnormal TAT and PIC levels in the acute phase then tended to become normalized during the convalescent phase of the disease. These findings indicated that activation of intravascular coagulability had occurred, with patients entering a temporary clot-forming state. Among the several hypotheses for the etiology of Bell's palsy, our findings support a circulation disorder as an influential factor.
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PMID:Intravascular hypercoagulability in patients with recent Bell's palsy. 798

We studied the effect of antiplatelet therapy not only on the secondary prevention of stroke but also on the suppression of vascular damages in patients with cerebral thrombosis at the chronic phase. We measured von Willebrand factor (vWF) as a marker for the endothelial system, and coagulation and fibrinolytic parameters in addition to platelet functions. The platelet aggregation and markers for platelet activation were monitored for the adequate inhibition of platelets. Twenty-one patients were treated with 200 mg ticlopidine. 9 patients with 100 mg ticlopidine and 60-150 mg acetylsalicylic acid, and 18 patients with 200 mg cilostazol daily. The mean duration of follow up was 8.4 +/- 3.0 months. A patient was attacked by a recurrent stroke, but no fatal vascular events occurred during the period. A significant decrease was observed in the collagen- and ADP-induced platelet aggregation and markers for platelet activation such as platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by the antiplatelet therapy. In addition, the activities of coagulation factor VIII (FVIII) and vWF, markers for vascular damages, showed a significant decrease. The results suggest that the antiplatelet therapy could ameliorate the vascular damage through the inhibition of platelet function. Moreover, thrombin-antithrombin III complex (TAT) and alpha 2-plasmin inhibitor-plasmin complex (PIC), markers for the activation of coagulation and fibrinolytic systems, decreased significantly, suggesting that the treatment inhibits the activation of coagulation and fibrinolytic systems induced by the platelet activation. The activities of FVIII and vWF decreased significantly when the level of beta TG or that of PF4 lowered sufficiently by the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antiplatelet therapy in patients with cerebral thrombosis at the chronic phase--assessment of its effect on coagulation and fibrinolytic parameters]. 799 82

We studied 84 consecutive patients referred with the suspicion of pulmonary embolism (PE) to investigate the influence of clinical and hematological profiles on the diagnosis and severity of this disease and recovery. Diagnosis of PE was confirmed in 48 out of 84 patients by perfusion scintigraphy and/or pulmonary arteriography. Severity of PE and entity of recovery were investigated by measuring standard PaO2 on blood gas analysis and the number of unperfused lung segments ULS on perfusion scintigraphy. Most common clinical predisposing conditions were more frequent, though not significantly so, in embolic patients and a very low prevalence of PE was appreciable in patients without clear predisposing conditions. Among coagulation factors, only thrombin-antithrombin (TAT) complexes were twice as high in embolic as in nonembolic patients (14.0 +/- 13.6 vs. 7.0 +/- 4.2 ng/ml; p < 0.02), while there was no statistically significant difference between embolic and nonembolic patients for activated partial thromboplastin time, prothrombin time, antithrombin III, protein C, fibrinogen, plasminogen, alpha 2-plasmin inhibitor, and plasminogen activator inhibitor-1. Sensitivity and specificity of TAT complexes in diagnosis of PE were 95.8% and 30.5%, respectively. Therefore, normal values of TAT complexes may help exclude the diagnosis of PE, while abnormal values allow to reinforce the clinical suspicion of PE. No relation was found between coagulation parameters and the severity of PE. The follow-up of 48 patients with confirmed PE was favorable on the average; however, neither the presence of predisposing conditions nor abnormal coagulation parameters allow to predict the degree of functional and scintigraphic improvement during follow-up.
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PMID:Clinical, anamnestic and coagulation data in patients with suspected or confirmed pulmonary embolism. 800 95

Recently it has been shown that tissue factor (TF), an important trigger for initiating blood coagulation, is present in the circulating plasma. In order to assess the clinical implications of TF in plasma, plasma concentration of TF was quantitated in 65 patients with disseminated intravascular coagulation (DIC). The mean concentration of plasma TF was elevated in patients with DIC at presentation as compared with healthy subjects (446 +/- SD 536 pg/ml vs. 138 +/- 51 pg/ml, P < 0.001). Abnormally high levels were found only in 46.2% of the patients, predominantly in patients with non-hematological solid tumors and acute leukemia. Plasma TF did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, prothrombin fragment 1 + 2, plasma-alpha 2-plasmin inhibitor complex, FDP, D-dimer, or fibrinogen. Serial determinations of plasma TF demonstrated that plasma TF changes roughly in parallel with the course of DIC in most patients with elevated TF at presentation of DIC. These findings suggest that plasma TF is potentially valuable for monitoring the progress of DIC in a limited population of patients.
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PMID:Tissue factor in plasma of patients with disseminated intravascular coagulation. 803 86

The effects of coronary thrombolytic therapy with urokinase on the intrinsic hemostatic and fibrinolytic states were investigated by determining several markers for hemostatic and fibrinolytic activities in 6 patients with acute myocardial infarction who underwent coronary thrombolysis with urokinase. The markers for hemostasis and fibrinolysis were: markers for plasmin generation [alpha 2-plasmin inhibitor (alpha 2-PI), plasminogen, plasmin alpha 2-PI complex (PIC)]; markers for fibrinolysis [fibrin/fibrinogen degradation products-E fragment (FDP-E), FDP D-D dimer (D dimer), fibrinogen]; markers for hemostatic activity (prothrombin time (PT), antithrombin III (AT-III), protein C); markers for thrombin generation [thrombin antithrombin III complex (TAT)]; markers for intrinsic fibrinolytic activity [tissue plasminogen activator plasminogen activator inhibitor complex (TPA PAI complex)]. These markers were measured before, at 1 to 2 hours intervals during first 6 hours, daily during the next 3 days, and subsequently on the 7th and the 14th day after urokinase therapy. Fibrinolysis (determined by increased D dimer) occurred only when alpha 2-PI became unmeasurable with 96 x 10(4) or more units of urokinase administration, then persisted for more than 2 hours. TAT increased from 13.1 +/- 15.4 to 70.8 +/- 65.8 ng/ml soon after fibrinolysis occurred, indicating that thrombin generation occurred at the same time as fibrinolysis. The TPA PAI complex level before urokinase administration (26.4 +/- 6.4 ng/ml) was greater than the normal upper limit, indicating increased intrinsic fibrinolytic activity, then decreased after urokinase administration. These findings suggested that urokinase administration might affect the intrinsic fibrinolytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serial changes in hemostatic and fibrinolytic states induced by coronary thrombolytic therapy]. 806 82

To screen for risk of embolism, we investigated the association between the presence of left atrial (LA) thrombus by transesophageal echocardiography (TEE) and blood coagulation tests, including thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor 1 (PAI-1), plasmin-alpha 2-plasmin inhibitor complex (PIC), D-dimer, tissue plasminogen activator (tPA), free tPA, tPA.PAI-1 complex, prothrombin fragment 1+2 and fibrin degradation product E (FDP-E) in 40 patients with atrial fibrillation (Af) (13 males, 27 females, mean age 76 +/- 8 yrs). Blood coagulation tests were performed in 21 control subjects with sinus rhythm (12 males, 9 females, mean age 75 +/- 4 yrs). LA thrombi were detected in the appendage of 8 patients and in the atrium of 6 patients. Severe atherosclerotic plaque with thrombi in the thoracic aorta were detected in 6 patients without LA thrombi. FDP-E, D-dimer and PIC increased significantly in patients with LA thrombi or aortic plaque in comparison with controls with sinus rhythm. In patients with Af, 25 of them (group A) has more than 4 abnormal coagulation values out of 9 tests and 15 of them (group B) had abnormalities in less than 3 tests. LA thrombi or aortic plaque were detected in 18 patients in group A and 2 patients in group B (72% vs 13%, p < 0.01). In 4 of 6 patients with large LA thrombi, the thrombi were resolved after administration of warfarin. Before administration of warfarin, tPA, PA-1 and tPA.PA-1 complex levels were higher in the two patients whose thrombi did not resolve.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Examinations to detect left atrial thrombus and blood coagulation test analyses in aged patients with atrial fibrillation]. 807 9


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