Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The thrombolytic action of commercial plasmin-Fibrinolysin, heparin and complex Fibrinolysin-heparin in thecom bination with the alpha-adrenoceptor agent DET was studied in rats. The induction of venous thrombosis is accompanied by the manifestations of disseminated intravascular coagulation (DIC). The most efficient thrombolytic action in the hypercoagulemic stage of DIC had the complex Fibrinolysin-heparin in the combination with DET. The alpha-adrenoceptor antagonist blocked the compensatory reaction on plasmin excess, liberated vascular plasminogen activator and thus increased and prolonged thrombo- and fibrinolytic effects of this complex. Administration of this complex in the combination with DET resulted in a steady hypocoagulation and hyperfibrinolysis in blood stream.
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PMID:Use of alpha-adrenoceptor antagonist dihydroergotoxin in experimental anticoagulant and fibrinolytic therapy. 245 12

Thrombotic thrombocytopenic purpura (TTP) is thought to be caused primarily by endothelial cell injury or primary platelet agglutination. A coagulation screen usually shows normal or minimal changes, but a modest elevation of fibrinogen/fibrin degradation products (FDP) is observed in many patients with TTP. To assess the thrombin generation in vivo in TTP, plasma levels of thrombin-antithrombin III complex (TAT) were measured together with plasmin-alpha 2-antiplasmin complex (PAP) in ten patients with acute TTP. Plasma TAT [mean 6.7 +/- (SD) 3.7 micrograms/liter] as well as PAP (2.1 +/- 1.2 mg/liter) were elevated in patients with TTP as compared with healthy subjects (TAT of 1.7 +/- 0.3 microgram/liter and PAP of 0.2 +/- 0.1 mg/liter; n = 10). These findings indicate that considerable amounts of thrombin and plasmin are actually generated in TTP, although the majority of patients do not show signs of consumption coagulopathy.
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PMID:Thrombin generation in patients with thrombotic thrombocytopenic purpura. 247 64

The effect of ONO-3307 (4-sulfamoyl phenyl-4-guanidinobenzoate methanesulfonate), a new protease inhibitor, was studied on various proteases in vitro and in an experimental thrombosis model in vivo. ONO-3307 competitively inhibited trypsin, thrombin, plasma kallikrein, plasmin, pancreatic kallikrein and chymotrypsin; and their Ki values were 0.048 microM, 0.18 microM, 0.29 microM, 0.31 microM, 3.6 microM and 47 microM, respectively. In addition, ONO-3307 inhibited both elastase release from N-formyl-Met-Leu-Phe (fMLP)-stimulated leukocytes and tissue thromboplastin release from endotoxin-stimulated leukocytes. To examine the effects of ONO-3307 on disseminated intravascular coagulation (DIC), we developed an experimental thrombosis model. ONO-3307 (10 mg/kg/hr) completely inhibited the deposition of radioactive fibrin in kidney and lung. Gabexate mesilate (50 mg/kg/hr) was also effective in this model, but the effect of nafamostat mesilate was unclear. These results indicate that ONO-3307 exhibits a wide range of inhibitory effects on various proteases, and ONO-3307 may be useful for the treatment of protease-mediated diseases such as thrombosis and DIC.
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PMID:Inhibitory effects of ONO-3307 on various proteases and tissue thromboplastin in vitro and on experimental thrombosis in vivo. 251 29

Detection of the cross-linked fibrin degradation fragment, D-dimer, in patients at risk for disseminated intravascular coagulation (DIC) is strong evidence for the diagnosis. D-dimer confirms that both thrombin generation and plasmin generation have occurred. Patients at risk for DIC (58) and normal controls (7) were studied. Thirty-three patients had DIC--with fragment D-dimer identified in their serum by immunoblotting. Latex agglutination measurements of fibrin(ogen) degradation products (FDPs) and D-dimer were compared with immunoblotting in the detection of D-dimer. FDP measurement was extremely sensitive but not specific. D-dimer measurement was less sensitive but highly specific. Used in tandem, screening with FDP and confirming with D-dimer, sensitivity and specificity were maximized, rendering a predictive value of a confirmed FDP of 100% in this cohort. D-dimer is a valuable adjunct for the laboratory diagnosis of DIC but is most appropriately used as a confirmatory test for the very sensitive FDP test.
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PMID:Diagnosis of disseminated intravascular coagulation. Role of D-dimer. 264 5

The treatment of disseminated intravascular coagulation (DIC) in infants with sepsis should be instituted after multimodality therapy of pyo-inflammatory diseases taking into account the degree of hemostatic disorders. In stage I DIC (hypercoagulation one), it is necessary to reach an adequate level of the inhibitors of the thrombin and plasmin systems. In this case it is quite sufficient to use donor's cryoplasma without heparin administration. In stage II DIC (transitory one) and stage III (hypocoagulation one), it is required that the drugs possessing antithrombin and antiplasmin activity, substitution therapy with blood preparations and components as well as measures to control hemorrhagic diathesis may be used.
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PMID:[Disseminated intravascular coagulation in newborn infants with infection]. 276 53

We present the case of a young man with acute monocytic leukemia (French-American-British classification:M5) and systemic hyperfibrinolysis with severe bleeding. Although fibrinolysis is usually mild and secondary to disseminated intravascular coagulation, its role as a primary and dominant factor in rare cases of leukemia warrants that its presence be sought as a cause of abnormal bleeding. Decreased serum plasminogen and increased serum plasmin determined by synthetic substrate assay and a negative protamine paracoagulation test are crucial findings. Use of high-dose epsilon-aminocaproic acid was effective in treating this complication. A transient increase in fibrinolytic activity coincident with the early effect of antileukemic treatment suggested that plasminogen activator and/or fibrinolytic protease substances were released from leukemic cells. Fibrinolytic activity subsequently disappeared with reduction in the population of leukemic cells.
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PMID:Primary fibrinolysis in acute monocytic leukemia. 276 88

We developed a new rapid assay for the factor XIa-alpha 1 antitrypsin in complex (F.XIa-alpha 1 AT) in plasma with the use of a newly produced anti-F.XI monoclonal antibody (KMXI-1). This assay was completed within about 5 hours, and the minimum assay range extended sensitivity about 5-fold over the former assay (Thromb. Res. 44, 489-501, 1986). In 20-fold diluted plasma samples, this assay was not affected by co-existing F.XI or nonspecific color development of the plasma. Normal levels of F.XIa-alpha 1 AT (11 +/- 4.1 ng/ml plasma [n = 96]) increased with the aging of healthy adults. The F.XIa-alpha 1 AT levels of patients with disseminated intravascular coagulation (DIC) rose along with the progression of the disease, and the appearance of high levels and the peak of F.XIa-alpha 1 AT developed faster than FDP-E or alpha 2 plasmin inhibitor-plasmin-complex in most patients. These results indicate that, in addition to FDP, F.XIa-alpha 1 AT is a useful molecular marker for DIC.
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PMID:New rapid assay for factor XIa-alpha 1 antitrypsin complex--application to DIC. 281 42

Plasma D-dimer was measured and compared with serum fibrinogen/fibrin degradation product levels (FDPs) in patients with disseminated intravascular coagulation (DIC) and other conditions associated with a hypercoagulable state. D-dimer (N less than 200 ng/ml) was elevated in all 43 patients with DIC, in 48 of 59 patients with liver disease, in 22 of 27 patients with acute leukaemia at presentation, in 17 of 23 patients with malignant disease, in 29 of 39 women in the third trimester of a complicated pregnancy, in 17 of 18 patients with deep venous thrombosis and in only four of 27 patients with acute myocardial infarction. There was a significant correlation between plasma D-dimer and serum FDP levels (P less than 0.01) as follows; DIC: r = 0.58, liver disease: r = 0.57, acute leukaemia: r = 0.84, malignancy: r = 0.87. The frequent elevation of D-dimer observed in liver disease, acute leukaemia, malignancy and complicated pregnancy indicates that a hypercoagulable state is a common occurrence in these conditions although in liver disease elevated levels resulting from a failure of normal clearance mechanisms cannot be excluded. The close relationship between D-dimer and FDP levels suggests that serum FDPs predominantly arise from the interaction of plasmin with crosslinked fibrin rather than with fibrinogen in the conditions in which these were compared.
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PMID:Plasma D-dimer levels and their relationship to serum fibrinogen/fibrin degradation products in hypercoagulable states. 291 30

In inflammation, particularly in septicaemia, complex coagulation disorders may lead to a dangerous haemorrhagic diathesis. The conventional concept for this syndrome called DIC implicates the occurrence of active thrombin in the circulation, which may be followed by hyperfibrinolysis due to plasmin formation. In this study data are presented suggesting an important role for a third proteolytic system, granulocytic elastase. The complexes of plasmin and elastase with their specific inhibitors, alpha 2-antiplasmin-plasmin (alpha 2AP-PI) and alpha 1-antitrypsin-elastase (alpha 1AT-ELP) were determined immunologically. The alpha 1AT-ELP appears mainly in gram-negative septicaemia, particularly in meningococcal disease. The estimation of alpha 2AP-PI and alpha 1AT-ELP, together with a method for the detection of the antithrombin III--thrombin complex which remains to be established, is a suitable tool for for the differential diagnosis of the consumption of coagulation proteins. The assumption that at least three proteolytic systems participate in the development of the haemorrhagic diathesis during inflammation leads to the concept of a broad, comprehensive substitution therapy with e.g. concentrates of AT III, PPSB, or fresh frozen plasma. The aim of this treatment is to replace not only the consumed procoagulatory factors, but also the lacking inhibitors in order to control this "abnormal proteolysis syndrome".
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PMID:The clinical significance of alpha 1-antitrypsin-elastase (alpha 1AT-ELP) and alpha 2-antiplasmin-plasmin (alpha 2AP-PL) complexes for the differentiation of coagulation protein turnover: indications for plasma protein substitution in patients with septicaemia. 293 57

Plasma and serum from patients with liver disease and elevated fibrin(ogen) degradation product (FDP) levels as measured by latex agglutination were analyzed by immunoblotting to characterize the FDP in these patients. An antihuman fibrinogen antibody was used that recognizes fibrinogen, fibrin monomer, soluble high molecular weight fibrinogen and fibrin polymers, as well as high molecular weight cross-linked degradation fragments, and the smaller fragments X, Y, D-dimer, D, and E. The analytic procedures were validated with plasma and serum from patients known to have intravascular fibrinolysis associated either with disseminated intravascular coagulation (DIC) or with thrombolytic therapy. The samples demonstrated a spectrum of plasmin degradation fragments on the immunoblots. Twenty-eight of 35 patients with liver disease (80%) had no evidence of plasmin degradation fragments in their plasma or serum. The cause of the elevated FDP levels as measured by latex agglutination was thought to be fibrin monomer or unclottable fibrinogen that was retained in the sera of some of these patients. Seven patients (20%) were found to have circulating plasmin degradation fragments. In addition to liver disease, however, these patients all had an illness (sepsis, shock, and pancreatic carcinoma) independently associated with intravascular coagulation and fibrinolysis. Three patients who lacked plasmin fragments also had pancreatic carcinoma or sepsis. The two groups of liver disease patients could not be clearly differentiated on the basis of clinical or laboratory evidence, but the blotting procedure proved to be a useful discriminator.
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PMID:Analysis of elevated fibrin(ogen) degradation product levels in patients with liver disease. 293 48


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