Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In 19 patients with chronic subdural hematoma, coagulation and fibrinolysis in venous blood taken at the time of surgery and in the hematoma contents aspirated from chronic subdural hematoma were studied. Compared with coagulation results for venous blood, the hematoma contents demonstrated marked prolongation of the recalcification time, prothrombin time, and activated partial thromboplastin time, and marked reduction of clotting factor V, the hepaplastin test, prothrombin, and fibrinogen. Antithrombin III was also decreased, and fibrinopeptide A was increased in the hematomas. Fibrinolytic results demonstrated that both plasminogen and alpha 2-plasmin inhibitor were decreased, and both fibrinopeptide B beta 15-42 and fibrin and fibrinogen degradation products were increased in the hematomas. These findings indicate excessive activation of the clotting system, thrombin generation, and increased fibrinolytic activity occurring in the hematomas. From these results, excessive activation of both the clotting and fibrinolytic systems is emphasized to be the possible etiological factor for the origin and development of chronic subdural hematoma.
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PMID:Coagulation and fibrinolysis in chronic subdural hematoma. 275 76

BRL 26921 (Eminase registered trade mark in Belgium, Germany and The Netherlands) is the p-anisoyl derivative of the primary (human) lys plasminogen-streptokinase activator complex (APSAC). The acyl-enzyme has the theoretical advantage of causing fibrinolysis in situ in the presence of fibrin clotbound plasminogen. It was administered to 34 patients with severe pulmonary embolism (PE) in an open multicentre study. PE was suspected on clinical, blood gas, ECG, and radiographic data. Pulmonary angiograms performed pre- and post-treatment confirmed the diagnosis and were assessed using the Miller Index (MI). Fibrinogen, plasminogen, alpha-2-antiplasmin, fibrinogen degradation products (FDP), activated partial thromboplastin time (APTT), partial thromboplastin time (PTT) were closely monitored before and after each administration of APSAC. Median angiographic improvement was 50% (range 0-94%). The following adverse events were reported: bleeding at puncture sites (n = 12), haematuria (n = 1), epistaxis (n = 3), fever (n = 2). A blood transfusion was given in one patient with an inguinal haematoma. Systemic fibrinogenolysis occurred in 20/28 patients.
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PMID:Thrombolytic treatment of pulmonary embolism with APSAC. 306 87

Hemorrhagic fever with renal syndrome in Korea (Korean hemorrhagic fever) is an acute viral disease characterized by fever, hemorrhage and renal failure. In Korean patients, the disease manifests more distinctive bleeding tendencies than those of hemorrhagic fever with renal syndrome found in western countries. To investigate the nature and role of the coagulation, fibrinolysis, kinin and immune system in the pathogenesis of such a hemorrhagic manifestation, alterations of these systems were assessed from the early phase of the disease. Decreased platelet count and shortened platelet survival were observed with giant platelets in the peripheral blood. The marked prolongations of bleeding time, prothrombin time and partial thromboplastin time were noticed with the decreased plasma activities of coagulation factors II, V, VIII, IX and X. Shortened half life of fibrinogen, increased fibrinogen-fibrin degradation product, with decreased plasma levels and activities of plasminogen, alpha 2-plasmin inhibitor and antithrombin III were found. On thrombelastogram, the existence of procoagulant activity was confirmed, and prolonged reaction time and clot formation time with decreased maximum amplitude were observed. The appearance of circulating immune complexes was found along with decreased C3 and normal C4 in the serum. Significant decrease of serum C3 was evident in the patients with disseminated intravascular coagulation. These findings of coagulopathy were normalized within ten days of the illness in most cases. Therefore, it can be concluded that disseminated intravascular coagulation and thrombocytopenia in the early phase, and azotemia developing later might play an important role in the pathogenesis of bleeding tendency in Korean hemorrhagic fever.
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PMID:Coagulopathy in patients with hemorrhagic fever with renal syndrome. 315 65

Blood coagulation and fibrinolysis in pregnancy with or without hyperlipidemia were studied. Blood samples were taken from 36 cases with early pregnancy, 59 cases with late pregnancy, and the relationship between the hemostatic changes and the concentrations of lipids was examined. The following results were obtained: 1. In early pregnancy, all cases were non-hyperlipidemic, but in 41% of late pregnancy cases, hyperlipidemia was found. 2. In late pregnancy without hyperlipidemia, shortening of prothrombin time and activated partial thromboplastin time, increases in platelet epinephrine, collagen aggregation, fibrinogen, and plasminogen, and a decrease in alpha 2-plasmin inhibitor were marked compared with those in early pregnancy without hyperlipidemia. 3. In late pregnancy with hyperlipidemia, the platelet count and fibrinogen were increased, and prothrombin and activated partial thromboplastin time were shortened compared with late pregnancy without hyperlipidemia. The platelet epinephrine aggregation was slightly decreased. Antithrombin III was increased and alpha 2-plasmin inhibitor was slightly decreased. 4. In the same subjects, the relationship between changes in blood coagulation and fibrinolysis in early and late pregnancies and total cholesterol was studied by the independent matched pair test. There were significant correlations (p less than 0.02, p less than 0.05) between activated partial thromboplastin time (r = -0.5998) and fibrinogen (r = 0.6230). From these results the author concluded that late pregnancy was a hypercoagulable state and this tendency was more obvious in late pregnancy with hyperlipidemia.
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PMID:[Hemostatic changes during pregnancy in reference to hyperlipidemia]. 339 35

The relationship between changes in blood coagulation and fibrinolysis during pregnancy and intrapartum-postpartum bleeding was studied as a trial prediction of abnormal bleeding during vaginal delivery in 27 subjects without any complications. The following results were obtained: In the third trimester, shortening of prothrombin time and activated partial thromboplastin time, increases in fibrinogen, platelet epinephrine, collagen aggregation, and plasminogen, and a decrease in alpha 2-plasmin inhibitor were marked as compared with those in the first trimester. In the same subjects, the relationship between changes in blood coagulation and fibrinolysis in the first and third trimesters and intrapartum-postpartum bleeding was studied by the independent matched pair test. There were significant correlations (p less than 0.005, p less than 0.001) between prothrombin time (r = -0.68862) and activated partial thromboplastin time (r = -0.77027). In the subjects whose prothrombin time and activated partial thromboplastin time in the third trimester were shorter than those in the first trimester, intrapartum and postpartum bleeding increased. The subjects whose prothrombin time and activated partial thromboplastin time in the third trimester were less by more than 0.52 seconds and more than 3.98 seconds, respectively, than those in the first trimester experienced abnormal bleeding exceeding 500 ml during delivery. In the intrapartum and postpartum bleeding group, shortening of prothrombin time and activated partial thromboplastin time, decreases in fibrinogen and alpha 2-plasmin inhibitor and an increase in platelet aggregation were more significantly observed than in the intrapartum and postpartum normal bleeding groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study of intrapartum and postpartum bleeding based on changes in blood coagulation and fibrinolysis during pregnancy]. 349 90

The influence of acute hypoxemia on blood fibrinolytic activity was investigated in 12 healthy males. Physiologically significant hypoxemia was produced by inspiration of 13% oxygen for 30 min. Six healthy males were exposed to hypoxemia at rest and 6 males to hypoxemia during exhaustive physical exercise on an ergocyclometer. During control experiments both groups of health males inspired 21% oxygen. In 5 patients with manifest respiratory insufficiency the effect of hypoxemia at rest was studied during withdrawal of oxygen treatment for up to 2.5 hours. No increase in fibrinolytic activity (measured with euglobulin clot lysis and fibrin plates) due to hypoxemia was observed either in resting healthy males or in patients. In healthy males the increase in fibrinolytic activity after physical exercise at 13% oxygen was even somewhat lower compared to 21% oxygen. No changes in other hemostatic parameters (activated partial thromboplastin time, factor VIII-related antigen, fibrinogen, plasminogen, alpha-2-antiplasmin, fibrin(ogen) degradation products) that could be attributed to hypoxemia, were observed in any group tested. It was concluded that short-term acute hypoxemia does not increase blood fibrinolytic activity in man.
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PMID:Acute hypoxemia does not increase blood fibrinolytic activity in man. 357 20

Sixty healthy men in three physical fitness categories (sedentary, on no organized fitness program; joggers, running 5-15 miles/wk; and marathoners, running greater than 50 miles/wk) were evaluated for changes in blood clotting and fibrinolytic activity before and after maximum exercise on a treadmill according to the Bruce protocol. The rate of blood clotting, as measured by prothrombin times, partial thromboplastin times and thrombin times, was accelerated by exercise (all P less than 0.005). The ability of euglobulin clots and plasma clots to lyse incorporated 125I-fibrin, termed 125I-euglobulin clot lysis (IEL) and 125I-plasma clot lysis (IPCL), were used as indexes of fibrinolytic activity. Marathoners had greater increases in fibrinolytic activity with exercise (76% compared with 63% for joggers and 55% for sedentary subjects by IEL; 427% compared with 418% for joggers and 309% for sedentary subjects by IPCL; all P less than 0.05). Fibrin degradation products increased with exercise (P less than 0.005 for the total group of 60 subjects). The absolute concentrations of alpha 2-plasmin inhibitor, alpha 2-macroglobulin, and antithrombin III increased with exercise (all P less than 0.005), but when concentrations were corrected for acute shifts of plasma water during exercise, the quantity of these inhibitors actually decreased (all P less than 0.005). The changes in clotting assays with exercise were not significantly correlated with changes in whole blood lactate, blood pyruvate, or rectal temperatures. Fibrinolytic assays before and after exercise correlated poorly to moderately with blood lactates (IEL: r = 0.441 and r = 0.425, respectively; IPCL: r = 0.294 and r = 0.544, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of exercise and conditioning on clotting and fibrinolytic activity in men. 359 18

Six coagulation proteins were measured in 79 consecutive patients referred to the coagulation service for suspected disseminated intravascular coagulation. Antithrombin III, plasminogen, and alpha 2-plasmin inhibitor were measured with fluorescent substrate assays. Fibronectin, prothrombin, and protein C were measured with electroimmunoassays. Using history and physical findings and the results of a coagulation screen (prothrombin time, partial thromboplastin time, fibrinogen, fibrin[ogen] degradation products, platelet count, and peripheral smear), the 79 patients were classified into five categories: no disseminated intravascular coagulation (n = 21), elevated fibrin(ogen) degradation products without other evidence of coagulopathy (n = 44), defibrination syndrome (n = 9), microangiopathic thrombocytopenic purpura (n = 4), and primary fibrinolysis (n = 1). Because the sensitivity and specificity of each of the proteins could not easily be compared, receiver operating characteristic (ROC) curves and areas under the ROC curves were calculated for each of the six proteins as well as for the tests of the coagulation screen. The ROC curves indicated that, apart from plasminogen, the other coagulation proteins provided little additional information about the classification of the coagulopathy.
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PMID:Diagnostic efficacy of six plasma proteins in evaluating consumptive coagulopathies. Use of receiver operating characteristic curves to compare antithrombin III, plasminogen, alpha 2-plasmin inhibitor, fibronectin, prothrombin, and protein C. 376 44

To clarify the hemocoagulative and fibrinolytic dynamics of the perinatal period and also to seek the cause of SGA (small for gestational age) baby birth, the coagulation and fibrinolysis of the cord blood were examined, and moreover a comparison with the maternal blood, discussion on the difference in birth weight, and an examination of the difference due to the sex of babies were made in 68 cases with full-term, vaginal, spontaneous delivery, and the following conclusions were reached. In comparison with maternal blood, cord blood significantly showed any of the following: Prolongations of the prothrombin time, and the activated partial thromboplastin time, a decrease in fibrinogen, and a decrease in the platelet aggregation, antithrombin III, and plasminogen. In addition, high values for thromboxane B2 and 6-ketoprostaglandin F1 alpha were observed. In the SGA group, significant decreases were observed in the platelet count, antithrombin III, plasminogen, and alpha 2-plasmin inhibitor as compared with the AGA (appropriate for gestational age) and LGA (large for gestational age) baby groups. No sex difference was observed in the hemocoagulative and fibrinolytic capacities of the cord blood. These hemocoagulative and fibrinolytic capacities, particularly changes in the fibrinolytic system observed in the SGA group, seem to be attributable to chronic DIC (disseminated intravascular coagulation) and mild acidosis due to various stresses during pregnancy and at parturition, in turn due to immaturity of the liver in babies.
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PMID:[Blood coagulation and fibrinolysis in cord blood with reference to birth weight]. 405 31

The function of fibrinolysis is to dissolve fibrin clots. The agent of fibrinolysis is plasmin, a glycoprotein with gram molecular weight (GMW) of 90,000. Under natural conditions, plasminogen is converted to plasmin by tissue plasminogen activator (TPA). Activation occurs on the fibrin surface, thus confining proteolytic activity to the appropriate site. Tissue plasminogen activator, produced by monoclonal methods, has recently been made available for limited therapeutic use. Currently streptokinase and urokinase are widely used therapeutically to activate plasminogen. These agents cause plasmin to be formed which is free in the circulation as well as bound to fibrin, resulting in proteolysis of circulating plasminogen and clotting factors. Fibrinolytic therapy has proven to be more beneficial than anticoagulation alone for deep vein thrombi and for pulmonary emboli. During therapy, laboratory studies demonstrate reduced concentrations of plasminogen, fibrinogen, and of alpha-2 plasmin inhibitor, and prolongation of activated partial thromboplastin time and thrombin time. Laboratory findings must be correlated with the clinical course. Demonstration of circulating plasmin-antiplasmin complex may be a useful indicator of active fibrinolysis.
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PMID:Fibrinolysis--a review. 623 87


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