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)

A study has been made of 31 patients with coronary heart disease where diagnosis had been clearly ascertained both from a clinical and strumental point of view. All patients had undergone aorto-coronary by-pass surgery. The controls of the parameters under observation (whole-blood and plasmatic viscosity, hematocrit, fibrinogen, euglobulin lysis, T protothrombin, T of partial thromboplastin, thromboelastogram antithrombin III, plasminogen, alfa2-macroglobulin and fractions C'3c, C'3c, C'4 of the complement) were carried out as follows: basic sample taken, I control (8th-10th day), II control (15th-20th day), III control (45th-50th day), IV control (85th-90th day) after surgical operation. A global examination of our results showed significant changes in the rheologic coagulative and fibrinolytic parameters after an aorto-coronary surgical operation. The slight tendency toward hypercoagulability met with in the basic blood sample (slight increase of whole-blood viscosity, hyperfibrinogenemy, inhibition of fibrinolytic activity) does not change significantly after surgical operation. This seems to indicate that the coronary by-pass does not in any way alter the evolution of arteriosclerosis.
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PMID:[Rheologic, coagulative parameters and study of fibrinolysis in patients with coronary heart disease before and after aorto-coronary by-pass (author's transl)]. 30 20

Antithrombin III is one of the main inhibitors in the blood coagulation mechanisms. Thrombin and factor Xa are slowly inactivated by it, as well as other serine proteinases of the coagulation mechanisms. Heparin tremendously accelerates the inhibitory function of antithrombin III. In the process antithrombin III activity is also reduced. Heparin retards the thrombin-fibrinogen reaction, but otherwise the effectiveness of heparin as an anticoagulant depends on antithrombin III in laboratory experiments, as well as in therapeutics. The activation of prothrombin is inhibited, and any thrombin or other vulnerable protease that might generate becomes inactivated. The measurement of antithrombin III concentration in blood is now achieved by research methods, as well as by methods that are practical for routine use. The tests require either thrombin or factor Xa as substrate, and could be specific for antithrombin III. There are congenital as well as acquired deficiencies of antithrombin III. The inhibitor is also found in tissues.
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PMID:Antithrombin III. Theory and clinical applications. H. P. Smith Memorial Lecture. 34 19

Thrombin or factor Xa added to plasma are inactivated by antithrombin III (At-III). The inactivation is accelerated by heparin, permitting assay systems which rapidly measure the At-III content of diluted plasma. Without heparin, the slow inactivation rates may be measured. Existing activity assays (fibrinogen or chromogenic substrates) and immunoassays of At-III have been reviewed. Correlation studies show a close correlation between the results of immunoassay and the results of most activity assays. In health, a narrow range of At-III has been found. The level is low in infancy. Fertile women have on the average somewhat lower levels than men. In old age, the level tends to drop. In clinical material studied with amidolytic assays, subnormal At-III levels were found in hereditary deficiency, liver disease, disseminated intravascular coagulation and in some cases with acute thrombosis. The amidolytic assays are rapid to perform, do not require experience in clotting technique and seem preferable in clinical routine work.
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PMID:Antithrombin III: critical review of assay methods. Significance of variations in health and disease. 35 Jul 29

Plasma levels of antithrombin III, alpha 2-macroglobulin and inter-alpha-trypsin inhibitor, as well as those of various clotting, complement and other plasma factors, were significantly decreased in 18 patients suffering from hyperdynamic septic shock. A similar statistically significant reduction of the concentrations of several plasma factors (prothrombin and antithrombin III, plasminogen and alpha 2-plasmin inhibitor, complement factor C3 and clotting factor XIII) was observed in experimental endotoxaemia. In this model the reduction in the plasma levels of these factors was considerably diminished by the intravenous injection of a granulocytic elastase--cathepsin G inhibitor of lower molecular weight from soybeans. The results of both studies indicate that consumption of plasma factors in the course of Gram-negative sepsis proceeds not only via the classical routes (by activation of the clotting, fibrinolytic and complement cascades by system-specific proteinases such as thrombokinase or the plasminogen activator) but also to an appreciable degree of unspecific degradation of plasma factors by neutral proteinases such as elastase and cathepsin G. The endotoxin-induced release of both sorts of proteinases, the system-specific ones and the unspecific lysosomal proteinases from leucocytes and other cells, is likely to be mainly responsible for the consumption of antithrombin III and alpha-2-macroglobulin via complex formation (followed by elimination of the complexes) and the increased turnover of the inter-alpha-trypsin inhibitor as observed in the clinical study. The therapeutic use of an exogenous elastase--cathepsin G inhibitor in the experimental model was stimulated by the observation that human mucous secretions contain and acid-stable inhibitor of the neutral granulocytic proteinases, called HUSI-I or antileucoproteinase. This inhibitor protects mucous membranes and soluble proteins against proteolytic attack by leucocytic proteinases released in the course of a local inflammatory response. Preliminary results indicate that HUSI-I, which is produced by the epithelial cells of mucous membranes, does not belong to any known structural type of acid-stable proteinase inhibitor. The search for other candidates suitable for medication in humans led to the discovery of a potent elastase--cathepsin G inhibitor, called eglin, in the leech Hirudo medicinalis. This acid-stable inhibitor with a molecular weight close to 8100 has an unusual structural property in that the structure of the molecule is not stabilized by any disulphide bridge.
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PMID:Proteinase inhibitors in severe inflammatory processes (septic shock and experimental endotoxaemia): biochemical, pathophysiological and therapeutic aspects. 39 95

The levels of components of the coagulation mechanism and fibrinolytic system in 20 hyperthyroid patients and 9 hypothyroid patients were compared with those of 20 euthyroid control subjects. The mean levels of fibrinolytic activity and plasminogen were significantly reduced in the hyperthyroid patients while mean levels of alpha1-antitrypsin and C1 inactivator were increased. Patients with hypothyroidism had significantly increased levels of fibrinolytic activity and alpha2-macroglobulin, a prolonged partial thromboplastin time, and reduced levels of factor XII and antithrombin III.
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PMID:Coagulation and fibrinolysis in thyroid disease. 41 38

Four different heparin assay methods were compared. Only procedures which can be routinely carried out in clinical laboratories were taken into consideration. A range of heparin concentrations was chosen for these tests which is likely to be expected in low dose heparin prophylaxis. The lowest sensitivity was found when the thrombin clotting time was applied, and slightly better results were obtained by the aPTT method. Addition of purified antithrombin III to the reaction mixtures improved the sensitivity of both methods. When factor Xa was used in a clotting test, the results were comparable to the aPTT method. The sensitivity was however, about 10 times higher when the remaining factor Xa was directly measured in a photometric assay system with a chromogenic substrate. The advantages and disadvantages of the different methods and the usefulness of heparin assays for clinical purposes are discussed.
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PMID:[Heparin assay in plasma. Comparison of different methods (author's transl)]. 46 52

Plasma exchange has been proposed as a treatment for multiple disorders. Three patients with amyotropic lateral sclerosis, who were hemostatically normal, were studied through a total of 11 4-liter exchanges. Plasma was replaced by an equal volume of 5% albumin or 5% plasma protein fraction. Serial studies revealed that immediately after the exchange transfusion, there was significant prolongation of the prothrombin, partial thromboplastin, and thrombin times with reduction of the fibrinogen and antithrombin III levels. Factors V, VII-X, IX, and X were all significantly decreased, as were the factor VIII antigen, procoagulant, and the ristocetin cofactor activities. Platelet counts were obtained before and after exchanges and revealed significant decreases. Four hours after exchange, all parameters remained abnormal except the factor IX, ristocetin cofactor, and factor VIII procoagulant activities. By 24 hr, all hemostatic parameters had returned to normal. These studies indicate that plasma-exchange transfusion with material devoid of coagulation factors results in a coagulation defect that may be of clinical significance in a hemostatically compromised patient.
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PMID:The hemostatic imbalance of plasma-exchange transfusion. 46 36

Blanket serial controls are not necessary in low-dosage heparin treatment. It would, in any case, be difficult under normal clinical conditions and would run counter to the whole conception of low-dose heparin treatment. However, in problem cases with an increased thrombo-embolic risk, sensitive methods for monitoring the heparin effect are recommended. A study on 150 patients has indicated that the most sensitive method is the use of chromogenic substrates. Thrombin time, using low-concentration thrombin solution of 1.5 NIH units/ml, thrombelastogram and activated partial thromboplastin time are less sensitive. Antithrombin III levels should be determined in all cases of increased heparin tolerance. With reduced antithrombin III levels and higher body weight an increase of the standard dose from 5000 U.S.P. units heparin t. i. d. subcutaneously to 7500 U.S.P. units t. i. d. should be considered.
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PMID:[Does low-dosage heparin treatment require serial haematological controls? (author's transl)]. 47 60

The precise quantitation of activated factors in human factor IX concentrates has been accomplished with the use of recently developed, specific assays for factors IXa, Xa, and thrombin. The assay for factor IXa, which measures the initial rate of 3H-factor-X activation, was shown to be specific for factor IXa in the concentrates. Activated factor IX concentrates contained 1.0-2.3 microgram/ml of factor IXa; whereas the assays of unactivated concentrates were negative (less than 0.2 microgram/ml). The assays of factor Xa and thrombin, which measure the initial rate of p-nitroaniline release from S-2222 and S-2238, respectively, showed similar small amounts of factor Xa (4-34 ng/ml) and thrombin (12-76 ng/ml) in the activated and unactivated concentrates. The nonactivated partial thromboplastin time of the concentrates correlated significantly with the factor IXa content, but not with factor Xa or thrombin. Antithrombin III antigen in 3 of 4 concentrates was several-fold higher than antithrombin III activity, suggesting the presence of antithrombin III complexed with activated factors. These results support the hypothesis that the degree of activation of factor IX concentrates is related primarily to the concentration of factor IXa, which may be responsible for the thrombogenicity of these concentrates in some clinical settings.
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PMID:Activated clotting factors in factor IX concentrates. 49 95

Fourteen patients with a documented sudden neurosensory hearing loss and four patients with other diseases causing neurosensory hearing loss were studied. The standardized coagulation workup included hematocrit, activated partial thromboplastin generation time, thrombin generation, prothrombin time, phase platelet count, platelet adhesivity, protamine sulfate, serum antithrombin III activity, fibrinogen, and Factor VIII values. Ony those patients having documented evidence of a neurosensory hearing loss occurring within hours or days were included in this study. Eight of the 14 paitents with a documented sudden neurosensory hearing loss satisfied our laboratory criteria for a diagnosis of in vitro hypercoagulability. Three of these patients had abnormal thrombin generation values, 4 had abnormal serum antithrombin III values, and 1 had an elevated platelet count. Four other patients with other diseases causing neurosensory hearing loss did not show evidence of in vitro hypercoagulability. It would appear from this data that coagulation abnormalities play a role in the pathogenesis of sudden neurosensory hearing loss.
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PMID:Hypercoagulability as a cause of sudden neurosensory hearing loss. 50


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