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)

The authors evaluated elements of the coagulation and fibrinolytic systems in 18 male patients with intermittent claudication vs 19 men matched for risk factors who served as controls. Prothrombin time and activated partial thromboplastin time did not significantly differ in the patients and the controls. The plasminogen level in the two groups was not significantly different. The level of lipoprotein(a) was significantly higher in the patients than in the controls. The levels of antigen and the activity of protein C did not differ significantly between the two groups. The thrombomodulin level was significantly higher in the patients than in the controls. There were no significant differences between the two groups in the levels of alpha 2-macroglobulin, C1-inactivator, or antithrombin III. The levels of fibrinogen and alpha 1-antitrypsin were significantly higher in the patients vs the controls. Significantly lower levels of alpha 2-plasmin inhibitor and higher levels of alpha 2-plasmin inhibitor/plasmin complex and thrombin/antithrombin III complex were found in the patients vs the controls. These findings suggest that the levels of thrombin/antithrombin III complex, alpha 2-plasmin inhibitor/plasmin complex, and thrombomodulin may perhaps serve as indicators for injury to the peripheral endothelium and that the coagulation and fibrinolytic systems may be activated in patients with intermittent claudication.
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PMID:Evaluation of the coagulation and fibrinolytic systems in men with intermittent claudication. 867 28

Plasma levels of selected coagulation and fibrinolytic parameters (activated partial thromboplastin time, prothrombin time, fibrinogen, antithrombin III, protein C, thrombin-anti-thrombin III complexes (TAT), plasminogen activator inhibitor-1 (PAI-1), plasminogen, alpha 2-plasmin inhibitor) were evaluated in 90 patients with clinical suspicion of pulmonary embolism (PE). Plasma levels of fibrinogen, PAI-1 and TAT were significantly higher in patients than in controls (p < 0.01): evaluation of TAT displayed a sensitivity of 96.1% and specificity of 30.8%, and positive and negative predictive values of 64.5 and 85.7%, respectively. The number of nonperfused lung segments correlated directly with TAT levels (p < 0.01) and inversely with arterial pO2 values (p < 0.01). No significant difference was found in the other parameters between patients and controls. Our results suggest that the finding of normal TAT plasma levels can help to exclude PE in patients with clinically suspected PE.
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PMID:Thrombin-antithrombin III complexes as an additional diagnostic aid in pulmonary embolism. 869 74

Seventy-four patients with PSS were evaluated with regard to plasma concentration of blood coagulation and fibrinolysis factors: fibrinogen (Fbg), prothrombin time (PT), active partial thromboplastin time (APTT), protein C, thrombin-antithrombin III complex (TAT), antithrombin-III (AT-III), factor XIII (XIII) fibrinopeptide A (FPA), alpha 1-antitrypsin (alpha 1-AT), plasminogen (Pmg), alpha 2-plasmin inhibitor plasmin complex (PIC), alpha 2-plasmin inhibitor (alpha 2-PI), alpha 2-macroglobulin (alpha 2-MG), fibrinopeptide B beta 15-42 (FPB beta-15-42) and soluble fibrin monomer complex (SFMC), FDP (fibrin degradation product) and D-dimer. They were also evaluated with regard to platelet-derived proteins: beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 and 6-keto-prostaglandin F1 alpha (6KF). In the coagulation/fibrinolysis systems high plasma levels of TAT, AT-III, FPA, alpha 2-MG and FPB beta 15-42 could be demonstrated in more than 50% of total PSS patients. There was no statistical correlation between those of TAT and AT-III. Plasma levels of PIC, D-dimer, FDP and SFMC were not always high. There was no statistical correlation between those of TAT and PIC. These data lead us to consider that alpha 2-MG may play an important role for inhibiting PIC, which accelerates the conversion from fibrin into FDP. Subsequently, there were high plasma levels of FPB beta 15-42 converted from fibrin monomer. These data seem to be indicative of an involvement of coagulation and platelet disorder in PSS. These platelet-vessel system disorders might be closely related to the pathophysiology of PSS.
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PMID:Plasma levels of molecular markers of blood coagulation and fibrinolysis in progressive systemic sclerosis (PSS). 878 74

High-altitude hypoxia causes polycythaemia and a hypercoagulable state in humans and animals. This study examines the effects of a hypobaric, hypoxic environment (HHE) on the blood coagulation system in rats. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m in altitude for 1-12 weeks. After 2 weeks of exposure to HHE, platelet counts decreased significantly; after 4 weeks, the prothrombin and activated partial thromboplastin times were significantly prolonged, compared with those of control rats. In addition, individual coagulation factors (VII, IX, X, XI, and XII) were significantly decreased at 8 weeks (P < 0.05). Levels of anti-thrombin III and alpha 2-plasmin inhibitor also decreased (between 4 and 8 weeks). After 4-12 weeks of exposure to HHE, 30 of 56 rats (54 per cent) developed (i) non-bacterial thrombotic endocarditis (NBTE) or (ii) infarction of the myocardium or kidney, or both (i) and (ii). The incidence of NBTE increased from 33 per cent (5/15 rats) at 4 weeks to 100 per cent (7/7 rats) at 12 weeks. Electron microscopy showed detached endothelial cells in the mitral valves at 1 week; platelets adhered to the subendocardial matrix and platelet aggregation with thrombus formation was seen at 2 weeks of exposure. The results suggest that exposure to HHE induces a hypercoagulable state and causes an NBTE in rats that may result in consumption coagulopathy.
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PMID:Hypercoagulable state in a hypobaric, hypoxic environment causes non-bacterial thrombotic endocarditis in rats. 915 22

The alterations of the haemostatic system (platelet count, activated partial thromboplastin time [APTT], thromboplastin time [standard test, modified test], thrombin time, fibrinogen concentration, activity of the coagulation factors II, V, VII, X, VIII:C, IX, XI, XII, of prekallikrein, high molecular weight kininogen, antithrombin III, protein C, plasminogen and alpha 2-plasmin inhibitor, concentration of soluble fibrin and fibrin(ogen) degradation products [FDP], resonance thrombogram) were described in seven dogs with haemorrhagic diathesis in consequence of an infiltrative, growing mammary carcinoma with multifocal invasion of lymphatic and blood vessels. In most of the cases metastases in different organs could be demonstrated. In every case a serious stage of disseminated intravascular coagulation and hyperfibrinolysis was existent. This was indicated by the distinctly increased concentration (p < 0.0001) of soluble fibrin (27.7 [16.0-79.2] micrograms/ml, median [minimum-maximum], reference range [RR.]: < 9.4 micrograms/ml) and FDP (340 [50-860] micrograms/ml, RR.: < 18 micrograms/ml) as well as a diminished plasma level of nearly all components of the coagulation and fibrinolytic system concerning especially the concentration of fibrinogen (0.16 [0.01-0.46] g/l, RR.: 1.17-3.09 g/l), the activity of factors V (30 [21-40]%, RR.: 75-158%) and VIII:C (9 [4-16]%, RR.: 72-136%) as well as the activity of protein C (8 [3-13]%, RR.: 68-139%) (each: p < 0.0001).
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PMID:[Disseminated intravascular coagulation and hyperfibrinolysis in dogs with metastasizing mammary carcinoma]. 986 56

Achieving early, complete, and sustained reperfusion after acute myocardial infarction does not occur in approximately 50% of patients, even with the most potent established thrombolytic therapy. Bleeding is observed with increased concentrations of thrombolytics as well as with adjunctive antithrombotic and antiplatelet agents. A novel approach to enhance thrombolytic therapy is to inhibit the activated form of thrombin-activatable fibrinolysis inhibitor (TAFI), which attenuates fibrinolysis in clots formed from human plasma. Identification of TAFI in rabbit plasma facilitated the development of a rabbit arterial thrombolysis model to compare the thrombolytic efficacy of tissue-plasminogen activator (tPA) alone or with an inhibitor, isolated from the potato tuber (PTI), of activated TAFI (TAFIa). Efficacy was assessed by determining the time to patency, the time the vessel remained patent, the maximal blood flow achieved during therapy, the percentage of the original thrombus, which lysed, the percentage change in clot weight, the net clot accreted, and the release of radioactive fibrin degradation products into the circulation. The results indicate that coadministration of PTI and tPA significantly improved tPA-induced thrombolysis without adversely affecting blood pressure, activated partial thromboplastin time, thrombin clotting time, fibrinogen, or alpha-2-antiplasmin concentrations. The data indicate that inhibitors of TAFIa may comprise novel and very effective adjuncts to tPA and improve thrombolytic therapy to achieve both clot lysis and vessel patency.
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PMID:A novel approach to arterial thrombolysis. 1051 77


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