Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well known that abnormalities of coagulation and fibrinolysis frequently take place during the course of cerebrovascular diseases. In this paper, coagulation and fibrinolytic studies were performed during the course of acute stage through chronic stage of subarachnoid hemorrhage. Tested items were partial thromboplastin time, prothrombin time, FDP, alpha 2-plasmin inhibitor, antithrombin III, fibrinogen, besides, fibrinopeptide A (FPA), and fibrinopeptide B beta (FPB beta) which were being worthy of note. Blood were sampled from peripheral vein (V) and internal jugular vein at jugular bulb (J). And, moreover, cerebrospinal fluid (L) were collected as possible as we could for measuring FPA and FPB beta. The obtained results were summarized as follows; Within forty-eight hours from the onset of subarachnoid hemorrhage, FPA-V, J,L and FPB beta-V, J,L were statistically higher than those of control. FPA-J and FPB beta-V, J, within forty-eight hours from the onset were statistically higher in the cases with brain death than in the survived cases. On the third to fifth day from the onset when so called cerebral vasospasm became apparent to begin, FPA and FPB beta had a tendency to be higher than other periods. Increase of fibrinogen delayed from the peaks of FPA and FPB beta showing the peaks at the seventh to the fourteenth day from the onset of subarachnoid hemorrhage. In three cases with symptomatic vasospasm, FPA and FPB beta showed maximal values two to four days prior to the appearance of symptomatic cerebral vasospasm. Other tests were all within normal limits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coagulation-fibrinolysis abnormalities in acute stage of subarachnoid hemorrhage (Part 1)--With special reference to the relation between cerebral vasospasm and fibrinopeptides A and B beta]. 651 24

Blood coagulation and fibrinolysis were studied in 65 patients with chronic myeloproliferative disorders (MPD). They consisted of 28 patients with chronic granulocytic leukemia (CGL) in chronic phase, 7 with CGL in blast crisis, 9 with polycythemia vera (PV), 13 with primary thrombocythemia (PTh) and 8 with primary myelofibrosis (MF). Hemorrhagic and thrombotic complications were observed in 19 and 8 patients, respectively. Activated partial thromboplastin time and prothrombin time were prolonged in many patients. Low factor II levels were observed in some CGL patients. Factor V was decreased in CGL patients in chronic phase and in PV patients. Fibrinogen was either normal or increased in most patients, but an elevation of fibrin/fibrinogen degradation products (FDP) was found in some patients. The VIIIR: Ag/VIII:C ratio was increased in CGL patients in blast crisis, in PV patients and in PTh patients. Antithrombin III and plasminogen were below normal in some patients. Most patients showed a decrease in alpha 2-plasmin inhibitor. These findings suggest that blood coagulation and fibrinolysis are involved in the pathogenesis of the thrombotic and hemorrhagic complications in these patients. Chronic low-grade intravascular coagulation might be present in some patients with MPD.
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PMID:Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders. 695 82

We had rare opportunities to examine changes in fibrin degradation products (FDP)-D-dimer (DD), thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC) and other coagulation parameters during the clinical courses of living-related partial liver transplantation (LRPLT). In seven out of eight recipients without severe rejection and/or disseminated intravascular coagulation (DIC), FDP-DD values reached their maximum at 5 to 10 days after transplantation, then gradually decreased. On the other hand, TAT values rose to the maximum at anhepatic or reperfusion phase of liver transplantation. These data represent hypercoagulation in consequence of tissue thromboplastin activation after extensive operation. Changes in PIC, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1) in the clinical course of case 1 suggested that fibrinolysis was suppressed by relatively elevated level of PAI-1 around the operation, but thereafter was adversely accelerated by relatively lower levels of PAI-1. In comparison with patients with DIC, TAT was much higher but PIC was significantly lower in recipients of LRPLT. These findings indicated that marked hypercoagulation and mild to moderate hyperfibrinolysis occurred in recipients of LRPLT.
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PMID:[Changes in coagulation parameters during the clinical courses of recipients of living-related partial liver transplantation]. 747 43

To assess the blood coagulative and fibrinolytic responses during cemented femoral neck replacement, we measured these parameters in 9 patients, including anti-thrombin III (AT-III), prothrombin time (PT) and activated partial thromboplastin time (APTT) before surgery, just before packing bone cement and after the insertion of the prosthesis. We also measured thrombin-anti-thrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC), and D-dimer. A significant increase in APTT, and decrease in AT-III and PT were observed before the insertion of bone cement and prosthesis. The value of TAT and D-dimer increased significantly after the insertion of the prosthesis, but there were no significant changes in PIC. The data suggest that blood coagulation is activated after the insertion of bone cement and prosthesis into the femoral shaft, and in addition, the fibrinolysis is also accelerated secondary to the activation of the coagulation. Further investigations are needed to establish whether the activation of the coagulation induced by the cemented replacement exerts a great influence on the appearance of pulmonary thrombosis or circulatory depression.
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PMID:Blood coagulation and fibrinolytic activity during femoral neck prosthetic replacement using bone cement. 760 97

Many reports have indicated that oral contraceptives can increase the incidence of thromboembolic disorders. Norplant, an implant contraceptive containing levonorgestrel, has been developed recently. The aim of this study is to observe the effect of Norplant on some hemostatic parameters. The subjects in this study were divided into 5 groups. Group 1 (control) consisted of 25 female blood donors. Group 2 (N = 25), group 3 (n = 25), group 4 (n = 17) and group 5 (N = 20) consisted of subjects who had been using Norplant for 2, 3, 4, and 5 years, respectively. Prothrombin time, activated partial thromboplastin time, fibrinogen level, assay of F VII and X, antithrombin III activity, plasminogen activity, alpha 2-plasmin inhibitor activity and platelet aggregation test were done in all subjects. Our results showed that there was a significant difference (p < 0.05) on platelet aggregation induced by 10 microM of ADP between the control group and Norplant users for more than 2 years, while the other parameters did not differ significantly. It is concluded that 5 years users of Norplant did not alter blood coagulability, but increased platelet response to 10 microM of ADP.
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PMID:The effect of Norplant on some hemostatic parameters in Indonesian women. 788 84

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

Twenty-two patients on regular hemodialysis treatment suffering from renal anemia were treated with intravenous recombinant human erythropoietin (rhEPO) for more than 8 weeks. Before and 4 and 8 weeks after the start of rhEPO administration, we measured prothrombin time, activated partial thromboplastin time, fibrinogen (FBG), antithrombin III activity (ATIII), plasminogen activity (PLG), alpha 2-plasmin inhibitor activity (alpha 2 PI), alpha 2-plasmin inhibitor-plasmin complex (alpha 2 PIC), and cross-linked fibrin degradation products (XL-FDP) in citrated plasma to determine whether rhEPO treatment enhances coagulation and fibrinolytic activity. The pretreatment values of FBG, alpha 2 PIC, and XL-FDP were significantly higher than the normal control values. The pretreatment values of ATIII, PLG, and alpha 2 PI were significantly lower than the normal control values. Platelet count and FBG were significantly increased 4 and 8 weeks after treatment with rhE-PO. The prothrombin time was significantly shortened 8 weeks after rhEPO treatment, but the activated partial thromboplastin time did not change. PLG was significantly decreased 4 and 8 weeks after rhEPO treatment, and ATIII and alpha 2 PI were significantly decreased 8 weeks after rhEPO treatment. alpha 2 PIC was significantly increased 8 weeks after rhEPO treatment, and XL-FDP was significantly increased 4 and 8 weeks after rhEPO treatment. These data suggest that in patients on regular hemodialysis treatment coagulation and fibrinolysis are already enhanced before the start of rhEPO treatment and that rhEPO administration further enhances these disorders.
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PMID:Enhanced coagulation and fibrinolysis during treatment with recombinant human erythropoietin in patients undergoing chronic hemodialysis. 804 58

The purpose of this study was to investigate whether or not the systems of coagulation and fibrinolysis are activated after human recombinant erythropoietin therapy in patients with end-stage renal failure and renal anemia. Six thousand IU of human recombinant erythropoietin (EPOCH) were administered intravenously to 11 patients once a week for 8 weeks. Coagulation, fibrinolysis and platelet as well as renal functions were investigated before and after the EPOCH therapy. Platelet count did not increase in spite of improvement in anemia. No changes in prothrombin time, activated partial thromboplastin time, concentrations of fibrinogen, fibrinopeptide A, thrombin antithrombin III complex, fibrin/fibrinogen degradation products (FDP), FDP-E, FDP-D dimer, plasmin alpha 2-plasmin inhibitor complex were observed. Platelet factor 4 and beta-thromboglobulin also were unchanged. Reciprocal changes in serum creatinine concentrations over the duration of therapy were compared before and after therapy. There was no significant difference between the reciprocal changes in serum creatinine concentrations before and after therapy. The increases in hemoglobin did not correlate with the changes in coagulation, fibrinolysis and the other parameters, except for the change in prothrombin time. These results indicate that coagulation, fibrinolysis and platelet systems in end-stage renal failure patients were not affected by EPOCH administration, in spite of increase in hemoglobin.
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PMID:Effects of recombinant human erythropoietin (EPOCH) on the coagulation and fibrinolytic systems and platelet function in pre-dialysis patients with chronic renal failure. 825 11

We studied the effect of hemodilutional autotransfusion on coagulative-fibrinolytic dynamics and metabolic response. Hemodilutional solutions used were Dextran-40 (group A) and Salin-HES (group B). The activated partial thromboplastin time (APTT) immediately after hemodilution was prolonged in both groups. Prothrombin time (PT) and hepaplastin decreased significantly, and a remarkable variation was observed particularly in group A. The results suggest that effect on fibrinolytic dynamics is not exerted in either group because antithrombin-III (AT-III) and fibrinogen decreased significantly, while fibrinogen degradation products (FDP) are within normal ranges, and plasminogen as well as alpha 2-plasmin inhibitor (alpha 2-PI) decreased significantly. On the other hand, all other parameters such as lactic acid level, pyruvic acid level in blood, lactic acid pyruvic acid ratio, and blood glucose level were elevated during surgery, but no difference was observed regarding these parameters between the two groups.
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PMID:[Effect of hemodilutional autotransfusion on coagulative-fibrinolytic dynamics and metabolic response]. 851 43

The sole administration of urokinase causes no initial prolongation of activated partial thromboplastin time (A-PTT), but thereafter produces serious progressive prolongation of A-PTT; it also causes a progressive, severe decrease in fibrinogen levels and alpha 2-plasmin inhibitor activity by depletion. The antithrombogenicity of urokinase is not caused by prevention of blood coagulation system activation by antithrombin effect, but by secondary fibrinolysis by plasmin. Consequently, the administration of urokinase as a sole anticoagulant results in activation of coagulation and fibrinolysis, and, as a result, induces disseminated intravascular coagulation. Therefore, it is concluded that administration of urokinase is an inadequate anticoagulation therapy unless it is combined with other antithrombin agents.
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PMID:Danger of urokinase as an anticoagulant with left ventricular assist devices. 857 15


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