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)

Acute promyelocytic leukemia (APL) is characterized by proliferation of morphologically abnormal promyelocytes and a severe bleeding diathesis. The abnormal promyelocyte is characterized by abundant, large granules, many of which are spindle-shaped. Electron microscopic appearance of the granules closely resembles that of Auer rods. The granules appear to possess tissue thromboplastin activity by both immunologic and clotting assays. Coagulation studies in APL are generally consistent with disseminated intravascular coagulation. Prolongation of the prothrombin time and elevation of fibrinogen degradation products are the tests that are most commonly abnormal. Although occasional reports indicate a favorable response of the coagulopathy to drugs that inhibit fibrinolysis, the use of prophylactic heparin appears to be the treatment of choice. The response rate of APL to chemotherapy regimens that contain an anthracycline is comparable to that of acute myelogenous leukemia. The recent description of the 15;17 chromosomal translocation which may be pathognomonic for APL is only the second example of a chromosomal marker of human neoplasia. Marked elevation of serum vitamin B12 and B12 binding proteins appears to be another characteristic feature of APL. An in vitro cell line of APL cells has been demonstrated to have the capacity to differentiate to functional polymorphonuclear leukocytes, but the cause for the maturation arrest is unknown.
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PMID:Acute promyelocytic leukemia. 39 71

Levels of hypocoagulabity induced with coumarin derivatives (aconocoumarin) were determined in 10 patients Quick's test was used to calibrate commercially available thromboplastin reagents against a reference reagent. The results were then standardised in the form of a correct prothrombin ratio. It was found that comparable results could be obtained, even with poorly sensitive thromboplastins, by determining a thromboplastin sensitivity index and using it to convert the prothrombin ratio obtained with each thromboplastin into a "correct" ratio, i.e. one that allowed for the depressed sensitivity of the thromboplastin concerned. It was found that thrombotest was more sensitive than the commercial thromboplastins; it was also superior to the reference reagent in expressing the level of drug-induced hypocoagulability. Attention is drawn to the soundness of expressing prothrombin times in terms of the correct ratio to cut out the effect of variations in sensitivity on the part of commercial thromboplastins. At the same time, stress is laid on the superiority of thrombotest in the monitoring of oral anticoagulant therapy.
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PMID:[Control of anticoagulant therapy with coumarin derivatives. Evolution of the tests used and their standardization]. 39 92

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

We studied the coagulation and complement systems during Rocky Mountain spotted fever in Macaca mulatta experimentally infected with Rickettsia rickettsii. Ninety-one percent of monkeys infected intravenously with a high dose (10(6) plaque-forming units [pfu]) and 56% of monkeys infected with low doses (10(-1)-10(2) pfu) of R. rickettsii died after two to four days of illness. With the onset of fever and rickettsemia, animals developed hyperfibrinogenemia, mild thrombocytopenia, prolonged prothrombin and activated thromboplastin times, and increased serum fibrin/fibrinogen degradation products (FDP). Rickettsemia, thrombocytopenia, and FDP were greater in fatally ill monkeys than in survivors. Hemolytic titers of the second and third components of complement were not depressed except in a single surviving monkey that developed peripheral gangrenous ecchymoses at a time when both rickettsemia and agglutinating antibody were present. Thus, although activation and consumption of complement may occur during Rocky Mountain spotted fever, the hemostatic disturbances in fulminant infections seem to be a direct effect of the infectious vasculitis.
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PMID:Studies of the coagulation and complement systems during experimental Rocky Mountain spotted fever in rhesus monkeys. 40 34

In the present study, the coagulative and the fibrinolytic faculties of the Japanese monkey (Macaca fuscata) were investigated and compared with those of the human. Regarding the coagulative faculty, the plasmic fibrinogen level, prothrombin times, and partial thromboplastin times of the Japanese monkey were similar to those of the human, but the antithrombin level in the monkey was higher than that in the human. Regarding the fibrinolytic faculty, the simian plasminogen level was significantly higher than the human, but the simian, plasma clot and the euglobulin clot lysis times were extremely prolonged, which means that the Japanese monkey has a great fibrinolytic potential, but that it is difficult to activate. In addition, the human and simian reactivities of plasminogen to streptokinase were also investigated and compared.
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PMID:Comparative studies of coagulative and fibrinolytic faculties between the Japanese monkey and the human. 40 88

A 10-year-old boy had a severe lifelong hemorrhagic disorder that had necessitated more than 50 hospitalizations. Laboratory examination showed prolonged bleeding, clotting, partial thromboplastin, prothrombin, and thrombin times. These findings were due to a potent inhibitor of the thrombin-fibrinogen reaction. This inhibitor was similar to heparin in that it acted immediately and did not interfere with the coagulant activities of certain venoms. It differed from heparin in not being adsorbed to barium citrate or neutralized by protamine sulfate. The inhibitory effect was found in the alpha1-globulin fraction. It was identified immunologically and functionally as a double-banded alpha1-antitrypsin of a previously unreported phenotype. The inhibitory effects were depressed by trypsin and heterologous anti-alpha1-antitrypsin.
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PMID:Antithrombin Pittsburgh: an alpha1-antitrypsin variant causing hemorrhagic disease. 41 31

A prospective study of hemostatic abnormalities in 108 cancer patients was undertken at an oncology clinic in a university teaching hospital. Tests included Quick prothrombin time, activated partial thromboplastin time, thrombin time, platelet count, modified Ivy bleeding time, fibrinogen, fibrin degradation products (FDP), euglobulin lysis time, protamine sulfate test, and factor V, VII, VIII and X assays. Ninety-eight per cent of the patients had one or more abnormal coagulation tests. The commonest abnormalities were elevated fibrin degradation products and prolonged thrombin time. Thrombocytosis occurred in 57% of patients, hyperfibrinogenemia in 46%, thrombocytopenia in 11%, and non had hypofibrinogenmia. It is suggested that platelet count, fibrinogen concentration, and serum FDP assay are the most useful tests in assessing the hemostatic abnormalities in cancer patients, although thrombin time, factor V assay, and bleeding time may also be helpful. The peripheral blood smears of 53 patients were reviewed, and only one showed microangiopathic hemolytic anemia. The data illustrate that subclinical coagulopathy is relatively frequent in patients with malignancy.
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PMID:Hemostatic abnormalities in malignancy, a prospective study of one hundred eight patients. Part I. Coagulation studies. 42 Jan 61

A study of coagulation has been performed on 8 chronic renal failure patients receiving carbenicillin therapy. All showed a prolongation of the bleeding, recalcification, partially-activated thromboplastin, prothrombin and thrombin times. These findings suggest the presence of an anticoagulant with an heparin-like mode of action. In vitro tests suggest that carbenicillin may be this factor. We have also shown that the drug produces a disturbance in the normal polymerization process. The implications of these findings for the treatment of (CRF) patients with carbenicillin are discussed.
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PMID:Effects of carbenicillin on blood coagulation: a study in patients with chronic renal failure. 42 53

With the use of cohort labeling with 75Se-selenomethionine, simultaneous platelet, fibrinogen, and plasminogen survival studies were carried out in 8 patients with chronic alcoholic liver disease and in 5 normal subjects. Clinical features, liver function tests, coagulation and fibrinolytic system activities, and platelet function were also assessed. On the basis of platelet survival, the patients could be divided into two groups. Three patients had shortened platelet survival; they were all thrombocytopenic and had greater prolongation of the prothrombin time (PT) and activated partial thromboplastin time (PTT) than the other 5 patients. However, platelet turnover was decreased in all the patients, and there was no difference between the two groups with regard to fibrinogen or plasminogen survival nor in the in vitro evidence of disseminated intravascular coagulation (DIC). Fibrinogen survival was increased in 5 of the 8 patients. Plasminogen survival was normal in 6 patients and prolonged in 2 patients with very low plasminogen levels. The absence of increased fibrinogen turnover in the patients studied indicates that the abnormalities in coagulation tests were not due to consumption coagulopathy. The authors' studies suggest that, at least for patients with chronic stable alcoholic liver disease, the concept that the coagulopathy of liver disease is due to increased utilization of clotting factors should be revised with caution.
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PMID:The hemostatic defect of chronic liver disease. Kinetic studies using 75Se-selenomethionine. 42 8

Ether precipitation of globulins from the supernatant fraction of prothrombin complex concentrate, followed by adsorption on tricalcium phosphate and elution gives a beta2 fraction termed Bridge anticoagulant neutralizing agent (BANA). Although this is completely free of all known blood clotting factors, it improves recalcification time, PTT and thromboplastin generation of hemophilic plasma. It also counteracts the effect of factor VIII inhibitor. Ultrasonic elution produced more activity per mg N than did citrate elution. The possibility is discussed of incorporating BANA preparation in the routine fractionation of plasms without reduction in the yield of factor VIII or prothrombin comples concentrate.
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PMID:Ultrasonic purification of Bridge anticoagulant neutralizing agent (BANA) and a study on its effect on factor VIII inhibitor. 43 13


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