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)

Seven blood coagulation tests which may indicate a state of hypercoagulability or of chronic intravascular coagulation were assayed in 106 blood samples from 50 patients with chronic renal insufficiency or after renal transplantation. The following abnormal results were obtained: increased titer of fibrin(ogen) degradation products in 60%, abnormal fibrinogen immunoelectrophoresis in 49%, shortened partial thromboplastin time and whole blood clotting time in 45 and 37% respectively, prolonged thrombin time in 34%, increased cryofibrinogen level in 21% and positive protamine sulfate gelation test in 11%. The greatest number of abnormalities was found during the first week after transplantation and during transplant rejection, and the smallest in patients with stable transplant who were anticoagulated with warfarin. Partial thromboplastin times of less than 19 sec were associated in 3/4 patients with thrombosis of the renal artery or vein or with rejection. Rejections could be identified with high probability (p less than 0.001).
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PMID:[Proceedings: Hypercoagulability and compensated intravascular coagulation in chronic kidney insufficiency and after kidney transplantation]. 76 78

Improved methods are described to obtain bovine prothrombin, Factor IX, Protein C, and autoprothrombin III (Factor X, Auto-III) in purified form. The prothrombin had a specific activity of 4,340 Iowa units/mg. Theoretically, a preparation of clean thrombin should have a specific activity of 8,200 U/mg, because 47.08% of the protein in prothrombin is lost when thrombin forms. Such thrombin preparations have been obtained (Arch. Biochem. Biophys. 121, 372 (1967)). The prothrombin concentration of bovine plasma is near 60 mg/liter. Protein C, first isolated by Stenflo (J. Biol. Chem. 251, 355 (1976)), was found to be the precursor of autoprothrombin II-A (Auto-II-A), discovered earlier (Thromb. Diath. Haemorrh. 5, 218 (1960)). Protein C (Factor XIV) was converted to Auto-II-A (Factor XIVa) by thrombin. Digesting purified Auto-III with purified thrombin removed a small glycopeptide from the COOH-terminal end of the heavy chain to yield Auto-IIIm. Auto-III thrombin leads to Auto-IIIm + peptide. Auto-IIIm was not converted to the active enzyme with thromboplastin, and furthermore, inhibited the activation of purified native Auto-III with thromboplastin. Auto-IIIm was also not converted to the active enzymes when the procoagulants consisted of purified Factor VIII, purified Factor IXa, platelet factor 3 and calcium ions. The "activation peptide" released by RVV-X from the NH2-terminal end of the heavy chain and the active enzyme (Auto-Cm) were purified. Auto-III was also activated with purified RVV-X. The same "actid of Auto-Cm. Purified Factor IX developed anticoagulant activity when reacted with an optimum concentration of purified thrombin. A suitable reagent for the assay of Factor IX was prepared by removing prothrombin complex from anticoagulated bovine plasma and restoring the prothrombin and Auto-III concentration with use of the respective purified proenzymes.
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PMID:Improved procedures for the purification of selected vitamin K-dependent proteins. 78 72

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

Evidence of disseminated intravascular coagulation (DIC) was dought in normal baboons infused with autologous hemolyzed whole blood, preceded or followed by infusion of dextran (molecular weight, 70,000). Mean peak plasma hemoglobin following a rapid single injection was 370 mg/100 ml in 2 animals and 1,236 mg/100 ml in 1 animal, while levels during continuous 5 hour infusion in 2 animals averaged 326 and 474 mg/100 ml, respectively. Dextran infusion immediately preceded hemoglobin injection in 2 baboons and followed hemoglobin injection by 1 1/2 and 2 1/2 hours, respectively, in 2 baboons. Coagulation studies showed a moderate although significant fall in platelet count with prolongation of the partial thromboplastin time following hemoglobin infusion, and shortening of the thrombin time after dextran. Fibrin degradation products developed in four of five experiments after hemolysate injection. The induction of acute experimental hemoglobinemia results, therefore, in the development of coagulation changes consistent with milk DIC. Preliminary infusion of dextran (molecular weight, 70,000) may facilitate this response by either initiating the development or impeding the clearance of fibrin degradation products.
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PMID:Coagulation changes in baboons during acute experimental hemoglobinemia and dextran infusion. 80 56

Of the many techniques available for short-term support of the failing liver, a closed "isovolemic" method of exchange transfusions remains simple and safe. We used this method to exchange 143 U. of blood in eight patients in Stage III/IV hepatic failure; four patients had no previous underlying liver disease. Significant improvements of biochemical and coagulation parameters resulted. Serum bilirubin, glutamic oxaloacetic transaminase and, lactic dehydrogenase levels fell from a mean, 24.7 mg. per 100 ml., 3,100 mU. per milliliter, 2,796 mU. per millilter, respectively, to 10.9 mg. per 100 ml., 122.9 mU. per milliliter, and 558.5 mU. per milliliter, respectively, 6 to 12 hours following transfusion. Prolongation of serum prothrombin and thrombin times (over controls) of 31.1 and 30.1 seconds (mean) were markedly decreased to 3.2 and 6.1 seconds 6 to 12 hours following transfusion; partial thromboplastin times were decreased from a mean 196.4 seconds to 87.8 seconds after the same period. Levels of Factors VII, IX, and X were increased transiently. Correlations of exchange transfusion to reversal of coma and improvements in electroencephalograms were poor. Two patients in coma were subjected to major surgery following exchange transfusion; one patient survived vagotomy and hemigastrectomy for stress bleeding and one withstood a temporary baboon liver heterotopic transplant which aided in recovery from coma. We recommend isovolemic exchange transfusion as specific treatment for coagulation abnormalities and as an over-all aid in lowering the mortality rate of patients in hepatic coma. Marked improvements in homeostasis make major surgery feasible.
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PMID:Exchange transfusion and major surgery in acute hepatic failure. 82 26

A new case of congenital dysfibrinogenemia has been discovered in a 20 year old woman, who suffered from a severe postpartal hemorrhage after the delivery of her first child, followed by episodes of thrombosis. Coagulation studies reveal a prolongation of thrombin time, reptilase time was immeasurable. Thromboplastin time and partial thromboplastin time were slightly prolonged. Low fibrinogen levels were obtained by techniques, which depend on the coagulation velocity following addition of thrombin, while immunological procedures gave slightly diminished values of fibrinogen. Patients's fibrinogen had a moderate inhibitory effect on the fibrin formation in normal plasma. However, inhibitors of the fibrinogen-fibrin conversion could not be detected. Coagulation factors were normal, fibriolysis as well. The cause of the coagulation disorder was found to be a defect of the fibrinogen molecule, leading to an abnormal fibrin polmerization of patient's fibrin monomers. The release of the fibrinopeptides in the paperelectrophoresis was normal. The defect of the fibrinogen molecule did not protect from thrombotic complications. The same defect could be found in the lower scale in patient's father, 4 of her 7 brothers and sisters, and her son.
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PMID:Fibrinogen Marburg a new genetic variant of fibrinogen. 83 66

Alterations in coagulation factors have been reported during acute pancreatitis. Therefore the relationship of coagulation measurements to complications of pancreatitis was evaluated prospectively in 35 patients in whom 130 serial coagulation profiles were performed, consisting of fibrinogen, platelet count (PC), fibrinogen-fibrin-related-antigen (FR-antigen), prothrombin time (PT), partial thromboplastin time, thrombin time, euglobulin clot lysis, and Factors II, V and VII-X levels. During attacks of acute pancreatitis, over-all mean initial fibrinogen and PC of 268 mg. per 100 ml. and 214,000 per cubic millimiter rose significantly (p less than 0.005) to peaks of 362 mg. per 100 ml. and 477,800 per cubic millimeter by day 6 to 10. Mean initial FR-antigen of 4.8 microgram per milliliter rose to peak 7.4 microgram per milliliter on day 5. In 21 patients with mild pancreatitis, mean highest fibrinogen, PC, FR-antigen, and PT were 329 mg. per 100 ml., 361,500 per cubic millimeter, 5.3 microng per milliliter and 14.1 seconds. These values were significantly higher (p less than 0.05 to 0.01) in patients with severe pancreatitis, being 422 mg. per 100 ml. 528,000 per cubic millimeter, 13.7 microng per milliliter, and 15.5 seconds, respectively. Evaluation of the relationship of coagulation measurements to early clinical features showd that mean initial fibrinogen levels were significantly higher (p less than 0.05 to 0.01) in patients with initial amylase greater than 1,000 Somogyi units percent, serum glutamic oxaloacetic transaminase (SGOT) greater than 250 S.F.U. percent, and initial 72 hour PAO2 less than 75 mm. Hg. Early hypoxemia also correlated (p less than 0.05) with elevated initial FR-antigen levels. Impaired early renal function correlated (p less than 0.01) with elevated initial PC only. Early hypocalcemia did not correlate with coagulation measurements. These findings demonstrate that marked changes in coagulation parameters occur during acute pancreatitis and are related to over-all morbidity. Correlation of early coagulation measurements with amylase levels and with respiratory, renal, and hepatic dysfunction suggests that enzyme-related intravascular coagulation may be implicated in the pathogenesis of these complications of pancreatitis.
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PMID:The relationship of coagulation factors to clinical complications of acute pancreatitis. 85 Aug 68

Coagulation and fibrinolysis tests were performed in 14 patients with hydatidiform mole before any significant therapy was given and again, after evacuation of the mole, in eight instances. The results were compared with those found in a group of ten volunteers with normal pregnancies. The most frequent abnormalities in the problem cases were a shortening of the partial thromboplastin time and a prolongation of the thrombin time. From a total of seven cases with complete hematologic profiles before and shortly after evacuation of the mole, first showed important drops in platelets and fibrinogen. The most altered profiles occurred after expulsion of the mole in cases with important previous uterine activity. The findings suggested a latent state of hypercoagulability with higher turn over rate of fibrinogen and increased levels of fibrinogen-fibrin degradation products, that may exist even before the mechanism of expulsion begins. It was concluded that the alterations in coagulation and fibrinolysis seen in molar pregnancies most likely have a multifactorial pathogenesis, but the initiating causes must depend on several events taking place in the trophoblast itself and their consequences upon a very distorted intervillous blood circulation.
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PMID:Coagulation and fibrinolysis in molar pregnancy. 85 Nov 43

In experimental infections of guinea pigs with a virulent strain of Leptospira icterohaemorrhagiae widespread hemorrhages were observed. Thrombocytopenia, prolongation of prothrombin, thrombin, partial thromboplastin and coagulation times, decrease of plasma fibrinogen, factor V, factor VIII and the presence of fibrinogen degradation products were demonstrated. Treatment of infected guinea pigs with heparin prolonged life for two to three days. The histological observations revealed that the main lesion is a severe injury of the vasculature, mainly arteries, arterioles and capillaries. Most of the endothelial cells are affected or destroyed and the muscular fibers of arteries and arterioles are injured. With Martius-Scarlet-Blue, Weigert or Picro-Mallory stains it was demonstrated that the organization seen in the vessels is not all made of fibrin. The conclusion reached was that the hemorrhages observed in experimental leptospirosis in guines pigs are due to disseminated intravascular coagulation.
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PMID:The pathogenesis of leptospirosis I. Hemorrhages in experimental leptospirosis in guinea pigs. 86 35

The evaluation of the bleeding patient starts with the integration of data from the history and physical examination. From this results either one probable explanation that can easily be substatniated by laboratory studies or, as more commonly occurs in practice, several possibilities that are reasonable and must be investigated by more extensive laboratory tests. In either event, the initial laboratory evaluation usually includes examination of the peripheral blood and measurement of the platelet count, bleeding time, prothrombin time, partial thromboplastin time, and thrombin time. More specific laboratory tests are then performed if indicated.
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PMID:Evaluation of the bleeding patient. 87


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