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)

Human plasma alpha2-plasmin inhibitor in fibrinolytic states was studied using immunochemical methods and radioiodinated plasminogen. The concentration and activity of plasma alpha2-plasmin inhibitor decreased when urokinase was added to plasma in vitro or infused intravenously in man. The decrease was associated with the appearance of plasmin-alpha2-plasmin inhibitor complex which subsequently disappeared from the circulation in a short time. A decrease of other major inhibitors, such as alpha2-macroglobulin and alpha1-antitrypsin, was not observed when the amount of urokinase added or infused was relatively small, and conversion of plasminogen to plasmin was not extensive. The formation of plasmin-alpha2-macroglobulin complex was observed only when plasma plasminogen was activated with a larger amount of urokinase, and after most of the alpha2-plasmin inhibitor was consumed by forming complexes with plasmin. The formation of plasmin-alpha1-antitrypsin complex was not observed even in the highly activated plasma unless exogenous plasmin was added to the plasma. alpha2-Plasmin inhibitor was the only inhibitor of which the concentration in plasma was significantly decreased in patients with disseminated intravascular coagulation and fibrinolysis among the major plasmin inhibitors in plasma. The most reactive inhibitor for regulating plasma fibrinolysis very likely is alpha2-plasmin inhibitor.
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PMID:The behavior of alpha2-plasmin inhibitor in fibrinolytic states. 6 62

Fibrinogen was depleted in dogs injected with a single dose of bothropase even if pretreatment followed by a continuous infusion of antifibrinolytic drugs was performed during defibrination. The activation of the fibrinolytic system as a secondary effect of the defibrination syndrome induced by bothropase injection was blocked completely by aprotinin (Trasylol) but not by EACA. Plasmin activity in spite of the inhibition of plasminogen activator suggests that, either an excess of activator is released in circulation or a plasmin-antiplasmin complex is dissociated by the circulating fibrin, according to the hypothesis of Ambrus and Markus [1], and Back et al. [4] for the mechanism of fibrinolysis in vivo. An experimental model is suggested for the study of the fibrinolytic mechanism in vivo, by the association of defibrinating agents, antivenom and antifibrinolytic drugs.
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PMID:Experimental defibrination and bothropase: a study on the fibrinolytic mechanism in vivo. 14 12

One hundred and twenty-six patients with malaria (30 cases of P. vivax and 96 cases of P. falciparum) were studied for evidence of hematological coagulation and fibrinolysis abnormalities. Anemia associated with malaria was observed only in P. falciparum infections and there was no correlation between the degree of anemia and the percentage of parasitemia. Decreased hematocrit levels were found to be statistically significant in P. vivax infected patients (P greater than 0.05). Thrombocytopenia was observed in both P. vivax and P. falciparum malaria patients (P less than 0.001) and correlated with the degree of parasitemia (r = 0.974). Plasmin activity was normal in P. vivax malarial patients but it was significantly increased in patients with a P. falciparum of more than 5 per cent parasitemia. Coagulation profiles showed normal PT, aPTT, and TT in P. vivax infected patients while prolonged PT and aPTT were observed in P. falciparum infection which correlated with the degree of parasitemia (r = 0.0992). Coagulation factors V, VII, and IX were the most sensitive parameters in the expression of coagulation defects and most coagulation abnormalities were due to liver involvement. However, 2 of 20 complicated cases of P. falciparum showed evidence of disseminated intravascular coagulation (DIC).
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PMID:Hematological and coagulation studies in malaria. 140 63

Release of tissue plasminogen activator (t-PA) and its interaction with plasma protease inhibitors were studied in two patients with massive defibrination, one after electroshock and soft tissue injury and the other after complicated labor; both had very severe hemorrhage. Large quantities of free t-PA were present in the circulation for several hours. Complexes of t-PA with plasminogen activator inhibitor 1 (PAI-1), alpha 2-macroglobulin and C1-inhibitor were also observed. PAI-1 antigen rose dramatically in both patients, and complexes of t-PA with PAI-1 rose rapidly during the period of observation. In contrast, the complexes of t-PA with alpha 2-macroglobulin and C1-inhibitor, present initially, persisted for short periods only and disappeared when free t-PA disappeared from the circulation. Plasmin was generated initially, as indicated by the presence of plasmin-alpha 2-antiplasmin complexes. Plasma concentrations of alpha 2-macroglobulin, C1-inhibitor, antithrombin III, and alpha 2-antiplasmin were severely depleted initially, but rapidly returned to normal. The observations demonstrate that there is a major release of t-PA in such defibrinating patients, that there is a role for protease inhibitors other than PAI-1 in the regulation of endogenous t-PA, and indicate the great rapidity with which such free t-PA is complexed and cleared.
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PMID:Complexing of tissue plasminogen activator with PAI-1, alpha 2-macroglobulin, and C1-inhibitor: studies in patients with defibrination and a fibrinolytic state after electroshock or complicated labor. 168 22

To clarify the effects on blood coagulation-fibrinolytic system after transcatheter hepatic arterial therapy for cases of hepatocellular carcinoma (HCC), plasma levels of Plasmin-alpha 2PI complex (PIC), Ddimer and Thrombin-ATIII (TAT) before and after therapy were measured by EIA, in addition to other conventional coagulofibrinolytic parameters. In the group (9 cases) treated with intra-arterial injection of adriamycin, there were no significant changes of coagulofibrinolytic parameters except for Ddimer (P less than 0.05) which was elevated 1-2 days after therapy. However, only two cases in whom plasma PIC, Ddimer and TAT levels were clearly elevated before therapy, showed further marked elevation of those parameters after therapy. In the group (29 cases) treated with intra-arterial injection of adriamycin-lipiodol suspension, whether or not embolized with gelfoam, plasma PIC, Ddimer and TAT levels were significantly elevated (P less than 0.01) after therapy, as well as other conventional coagulofibrinolytic parameters. These results indicate that hypercoagulable and hyperfibrinolytic states were induced by treatment. Moreover, the secondary hyperfibrinolytic state tended to persist longer than the hypercoagulable state. The 14 cases embolized with gelfoam seemed to have more apparent effects on blood coagulation-fibrinolytic system than cases not treated with gelfoam. Therefore, we conclude that caution and prophylaxis for the occurrence of disseminated intravascular coagulation are necessary for transcatheter arterial therapy for cases of HCC.
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PMID:[Effects on blood coagulation-fibrinolytic system after transcatheter hepatic arterial therapy in cases of hepatocellular carcinoma analyzed by plasma levels of plasmin-alpha 2-PI complex, D dimer and thrombin-ATIII complex]. 169

Serial changes of activated factor XIII (XIIIa), alpha 2 Plasmin inhibitor (alpha 2PI) and fibronectin (FN), which have important role in wound healing and host defence mechanism, were studied in 27 trauma patients. We obtained the results as follows. 1) The alpha 2PI and the FN decreased in proportion to injury severity score (ISS) immediately after trauma and they increased statistically significantly on the second or the third hospital day. On the other hand the XIIIa showed no statistically significant changes after trauma. 2) Emergency operations performed on the first hospital day had no influence on the variations of the XIIIa, the alpha 2PI and the FN. 3) The patients with disseminated intravascular coagulation (DIC) showed statistically marked decrease of the XIIIa, the alpha 2PI, and the FN on admission and the first hospital day compared with those patients without DIC. On the second hospital day, there was no difference of these factors between the DIC patients and the patients without DIC, but on the following day the alpha 2PI and the FN decreased again. In conclusion, the alpha 2PI and the FN decrease in proportion to ISS but XIIIa shows no significant changes after trauma. Emergency operations have no influence on the variations of these factors but with complicating DIC, all of these factors decrease significantly.
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PMID:[Variation in wound healing factors in trauma patients]. 196 9

Thrombin-antithrombin III complex (TAT) and Plasmin-alpha 2 plasmin inhibitor complex (PIC) were examined in fifty two cases of various chronic liver diseases. TAT was significantly elevated in cases of hepatocellular carcinoma (HCC), but PIC did not show significant changes in any chronic liver diseases. Elevations of TAT and PIC were seen in cases of HCC accompanied by tumor enlargement and extensive tumor thrombosis. In cases of HCC undergoing transcatheter arterial embolization (TAE), TAT and PIC increased on the next day after TAE, and tended to recover with time, returning to almost normal at fourth week. Prolongation of prothrombin time, elevation of FDP and positive FM test were noted more often in liver cirrhosis with disseminated intravascular coagulation (DIC) than in severe liver dysfunction without DIC. Of five cases confirmed as DIC, only three cases were diagnosed as DIC by DIC score. On the other hand, TAT and PIC were significantly elevated in DIC cases. Especially, TAT exceeded 30 ng/ml in all DIC cases. TAT was regarded to be useful for the diagnosis of DIC in severe liver dysfunction.
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PMID:[Clinical significance of thrombin-antithrombin III complex and plasmin-alpha 2 plasmin inhibitor complex in chronic liver diseases]. 214 51

Plasmin-alpha 2-plasmin inhibitor (alpha 2PI) complex, an indicator of in vivo plasmin generation, was measured in the plasma of 48 patients with disseminated intravascular coagulation (DIC), by enzyme-linked immunosorbent assay (ELISA). Plasmin-alpha 2PI complex was markedly elevated to 7.9 +/- 4.26 mg/liter (mean +/- SD) in DIC at presentation, with normal values at less than 0.8 mg/liter. The concentration of plasmin-alpha 2PI complex changed in parallel with the course of DIC and decreased to 1.9 +/- 1.49 mg/liter (n = 28) in remission. Among various underlying disorders, DIC, in patients with acute promyelocytic leukemia, had the highest complex levels (mean 10.8 mg/liter), and septic patients had the lowest levels (mean 3.4 mg/liter). No significant correlation was found between FDP and plasmin-alpha 2PI complex. These results indicate that the quantitative assay of plasmin-alpha 2PI complex in plasma would be valuable in the assessment of hyperfibrinolysis in DIC.
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PMID:Plasmin-alpha 2-plasmin inhibitor complex in plasma of patients with disseminated intravascular coagulation. 245 7

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

Abnormalities of coagulation and fibrinolysis in 12 head-injured patients were studied in early (within 24 hours of onset) and late (10th to 17th day after onset) stages. alpha 2 Plasmin inhibitor (alpha 2PI), antithrombin III (ATIII), and fibrinopeptide A (FPA) and B beta 15-42 (FPB beta) were measured in particular, in addition to the usual tests (platelet count (PLT), prothrombin time (PT), partial thromboplastin time, fibrinogen, and fibrin/fibrinogen degradation products (FDP)). alpha 2PI was abnormally lower, and FPA and FPB beta were much higher; fibrinogen and ATIII were moderately lower in the early stage than in the late stage in 6 head-injured patients with postoperative intracranial hemorrhage. alpha 2PI, ATIII, and fibrinogen were moderately lower and FPA was moderately higher in the early stage than in the late stage in 6 head-injured patients without postoperative intracranial hemorrhage. PLT and fibrinogen were lower, alpha 2PI was much lower, and FPA was much higher in the 6 patients with postoperative intracranial hemorrhage than in the 6 patients without postoperative intracranial hemorrhage. One patient with acute epidural and subdural hematomas had recurrent postoperative intracerebral hematoma twice. This recurrent hemorrhage was due to disseminated intravascular coagulation (DIC) caused by primary brain damage and was associated with extremely high FPA and FPB beta levels and abnormally low alpha 2PI and PLT. Fresh-frozen plasma and intravenous low-dose heparin were administered after the two recurrent hemorrhages, after which FPA and FPB beta normalized immediately, although other screening tests showed only gradual improvement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between abnormalities of coagulation and fibrinolysis and postoperative intracranial hemorrhage in head injury. 378 92


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