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:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial thromboplastin time, thromboplastin time, plasma thrombin time, fibrinogen, thrombin-coagulase and reptilase times as well as platelet count. Normal values of these laboratory parameters were established for healthy newborns 1--5 days of age, and for healthy adults. It is suggested that especially partial thromboplastin time, the thrombin-coagulase and reptilase times, the latter influenced by fibrinolysis cleavage products, are representative for the tentative diagnosis of disseminated intravascular coagulation with fibrinolysis syndrome (DICFS). The platelet fall often lags 1--2 days behind the event. Moreover normal values for newborns, are markedly higher than those for older children or adults. In the presence of DICFS, a low-dose heparin therapy is immediately initiated. If completed defibrination is manifest, therapy is supplemented with urokinase and streptokinase, For DICFS with congenital sepsis, an exchange transfusion with heparinized fresh blood is the treatment of choice.
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PMID:[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)]. 32 24

We have tested a platelet aggregation inhibitor in the incubation fluid of deendothelialized fragments of the rat aorta and compared it with that of "intact" fragments. Some of the properties of the aortic inhibitor, and its effects on platelet adhesion to collagen fibrils, on platelet factor-3 (PF-3) availability, and on the activated partial thromboplastin time (APTT) and thrombin time (TT) were also evaluated in comparison with similar effects exerted by PGI2. We found that the incubation fluid of deendothelialized aortic samples contained inhibitor activity comparable with that of "intact" samples. The aortic inhibitor had similar properties to PGI2. The aortic inhibitor and PGI2 slightly inhibited light transmission changes of EDTA-PRP following exposure to collagen. However, scanning electron microscopy showed no appreciable difference in platelet adhesion to collagen fibrils. PGI2 and the aortic inhibitor inhibited Kaolin-induced PF-3 availability, but did not prolong the APTT or TT.
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PMID:Generation of a PGI2-like activity by deendothelialized rat aorta. 38 19

The vessel wall contains powerful inhibitors of thrombogenesis. One substance, a proteoglycan, is a strong anticoagulant but has only a limited effect on platelet aggregation. It prolongs the thrombin clotting time and partial thromboplastin time, but only blocks platelet aggregation induced by thrombin. Another vessel wall constituent, a prostaglandin derivative (prostacyclin), is a potent inhibitor of platelet aggregation. It antagonizes platelet aggregation induced by a variety of agents including adenosine diphosphate, collagen, arachidonic acid and thrombin; however, its only effect on coagulation is through the inhibition of platelet factor-3 release. Proteoglycans and prostacyclin comlement each other's antithrombotic activities, and together serve to limit the hemostatic response of blood to vessel wall injury. Vessels devoid of the intima continue to produce prostacyclin. Prostacyclin produced by these vessels is probably more important than that produced by vessels with the intima in the prevention of thrombus deposition.
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PMID:Vascular substances that modulate blood-to-vessel interactions. 39 10

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

The effects of three widely spaced levels of bacterial contamination of reagent water on several chemistry, radioimmunoassay, and coagulation procedures were studied. These included determinations of lactate dehydrogenase, creatine kinase, aspartate transaminase, alkaline phosphatase, blood urea nitrogen, total protein, thyroid-stimulating hormone, digoxin, thrombin time, activated partial thromboplastin time, and prothrombin time. Statistical analyses included calculations of means and coefficients of variation, and analysis of variance, as well as correlation coefficients for test results versus logarithm of bacterial contamination. Statistically and clinically significant differences occurred together only for an elevated level of creatine kinase.
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PMID:Effects of bacterial contamination of reagent water on selected laboratory tests. 43 36

Strenuous physical exercise leads to a significant shortening of blood clotting in various test systems. Such short times are also characteristic of those observed in sedentary patients with thrombosis or disseminated intravascular coagulation, and of those observed in experimental animals after thrombin infusion. The patients exhibit an increase in circulating fibrinopeptide A, which is attributed to thrombin action on circulating fibrinogen, and to an increase of fibrinogen degradation products, which is thought to indicate reactive fibrinolysis. To check whether physical exercise leads to fibrinemia, 10 healthy male volunteers were subjected to strenuous exercise on a bicycle ergometer. Blood samples were taken immediately before and on completion of the exercise period. Despite a significant shortening of the activated partial thromboplastin time, the thrombin time, and the Reptilase time, no increase of fibrinopeptide A could be demonstrated and the ethanol gelation test remained consistently negative. Simultaneously, the euglobulin lysis time was significantly shortened, whereas the fibrin(ogen) degradation products did not increase. The results indicate that the shortening of the coagulation times associated with physical exercise must be explained by mechanisms other than thrombin-mediated conversion of fibrinogen to fibrin.
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PMID:Lack of fibrin formation in exercise-induced activation of coagulation. 43 23

An automated method is presented for the determination of thrombin generation in plasma during activation by thromboplastin. The thrombin generated is allowed to split the chromogenic substrate Tol-Gly-Pro-Arg-pNA yielding p-nitroaniline. The increase in absorbance at 410 nm is recorded. This assay may serve as a specific, precise and fast alternative for the conventional clotting tests: "Prothrombin time" and "Thrombotest".
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PMID:An automated amidolytic assay of thrombin generation: an alternative for the prothrombin-time test. 43 85

The release of tissue thromboplastin after a severe brain injury can lead to a consumption coagulopathy. In a group of 83 patients with severe brain injury, platelet count, fibrinogen, prothrombin, partial thromboplastin time and thrombin time were investigated. The pathological laboratory findings in 14 were compatible with a consumption coagulopathy. These alterations were demonstrated during the first hours following trauma and represented an extra handicap for the patients who had to be treated surgically.
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PMID:[Secondary blood coagulation disturbances after severe head injuries (author's transl)]. 44 May 17


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