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)

Plasma fibronectin (Fn), a glucoprotein of suggested importance in host defence during infections also seems to be involved in blood coagulation and to be consumed during clot formation. Low Fn concentrations have been found in patients with DIC, but also in patients with infections without signs of overt DIC. In a randomized trial of Fn supplementation 28 patients with moderately severe infections, hospitalized in the Department for Infectious Diseases, were scheduled to receive either cryoprecipitate from 30 donors (n = 14) or 250-300 ml of stored plasma (n = 14). To elucidate the relationship between Fn plasma levels, Fn-rich cryoprecipitate infusion, and possible low-grade DIC in these patients, we measured platelet count, prothrombin complex (NT), fibrinogen, F V, F VIIIR:Ag, F VIII:C, F XII, plasminogen (Plg), antiplasmin (AP), antithrombin III (AT), kallikrein-inhibiting activity (KI) and spontaneous proteolytic activity (SPA). Compared to healthy controls, high initial values (p less than .001) were found for fibrinogen, F VIIIR:Ag, F VIII:C and SPA. Most values for platelets, F V, Plg, AP and KI were within the reference range. Low levels (p less than .001) were found for Fn, NT, F XII, AT and for the ratio F VIII:C/F CIIIR:Ag. A significant correlation was found between F XII, Plg and AT. Fn correlated poorly to the other variables. Cryoprecipitate infusion normalized the Fn concentration, but had no influence on other measured variables. Thus, although no patient had clinically overt DIC, and all survived, we observed a distinct pattern indicating activation of the coagulation system. Fn levels were low, but were not specifically related to this activation.
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PMID:Fibronectin and other DIC-related variables in patients with moderately severe infections receiving cryoprecipitate. 393 19

In a controlled study of fibronectin supplementation in sepsis, 11 ICU patients in septic shock were scheduled to receive either cryoprecipitate from 20-40 donors (n = 6) or 250-300 ml of stored plasma (n = 5) (two infusions over 24 h). We wanted to: compare some "conventional" DIC variables in the ICU (platelet count, prothrombin complex = NT, FDP) to additional variables: Fibronectin (Fn), fibrinogen (Fg), F V, FVIII R:Ag, F VIII:C activity, F XII, plasminogen (Plg), antiplasmin (AP), antithrombin (AT), kallikrein inhibiting activity (KI) and spontaneous proteolytic activity (SPA): study the effects of cryoprecipitate or plasma infusion on three variables. Samples were taken before the first infusion, and 24 and 48 h after. At onset, high levels (p less than .001 when compared to blood donors) of Fg, VIIIR:Ag and VIII:C were seen. KI levels were within the normal range. F V was low (p less than .05). Fn, NT, XII, Plg, AP and AT were markedly low (p less than .001). SPA showed great variation. When compared to 28 patients with severe infections, but not in septic shock, the ICU group had higher VIIIR:Ag (p less than .05) and VIII:C (p less than .01), and lower XII, Plg, AP and AT (p less than .001). FDP was elevated in all ICU patients. Five patients were thrombocytopenic, and in these a pattern with low levels of Plg and AT was observed. Fn did not correlate well to the other variables measured. These results indicate a marked activation of coagulation and fibrinolysis in these severely ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibronectin and other DIC-related variables in septic ICU patients receiving cryoprecipitate. 393 20

Since chickens are naturally deficient in several clotting factors normally present in mammalian sera, the ability of lead acetate (PbAc(2)) to sensitize 11-day-old chicks to endotoxin was compared with its ability to sensitize rats. It was found that, although the chicks could tolerate only relatively low doses of PbAc(2), even those doses would produce a greater than 200-fold sensitization to the endotoxin in rats, as compared with little sensitization in the chicks. By using larger doses of PbAc(2), known to maximally sensitize rats to endotoxin, the effect of PbAc(2) sensitization on whole-blood clotting times, platelet counts, plasma factor V and VIII activities, and the appearance of fibrin degradation products was evaluated. It was found that animals treated with lethal doses of endotoxin but no PbAc(2) showed varying degrees of consumptive coagulopathy. On the other hand, the injection of minute quantities of endotoxin into PbAc(2)-sensitized rats invariably resulted in disseminated intravascular coagulation, apparently via a complete activation of the intrinsic pathway. It is concluded that the site of PbAc(2) sensitization to endotoxin is in the blood, and most probably at the level of Hageman factor activation.
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PMID:Potentiation of endotoxin-induced consumptive coagulopathy by lead acetate administration. 461 26

Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease.
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PMID:Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis. 625 Apr 26

A fast migrating protein (FMP) was detected by agarose radio-crossed immunoelectrophoresis, in addition to factor VIII antigen (VIII:RAg), using antiserum to human factor VIII (FVIII). FMP had partial immunochemical identity with FVIII, migrated as an alpha-protein, and was distinct from alpha-2 macroglobulin, fibronectin or IgM. FMP was precipitated by concanavalin A and was separable from the bulk of VIII:RAg by ammonium sulphate fractionation. A significant amount of FMP was seen in normal serum (n = 12), plasma from patients with: (a) disseminated intravascular coagulation (n = 12) and (b) severe haemophilia A (n = 6). Trace amounts of FMP were observed in plasma from normal donors (n = 12), but neither VIII:ARg nor FMP was detectable in the plasma or serum from patients with severe von Willebrand's disease (n = 3). Freshly prepared cryoprecipitate contained trace amounts of FMP, similar to normal plasma, but increased levels were observed in antihaemophilic factor concentrates prepared for patient use. Significant levels of FMP were also seen in cryoprecipitate after storage at 4 degrees C for 7 d and this generation of FMP was diminished by the addition of protease inhibitors. The presence of significant levels of FMP in situations where proteolytic enzymes may be activated and inhibition of its generation by protease inhibitors, suggest that this protein is produced by proteolytic action of enzyme(s) on the FVIII molecule.
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PMID:Fast migrating protein, immunochemically related to human factor VIII, studied by crossed immunoelectrophoresis in agarose. 640 77

In 24 cirrhotic patients at different stages of hepatic failure, factor VIII:C (F VIII:C), factor VIIIR:AG (F VIIIR:AG), factor VIII AG/C ratio (F VIII AG/C), and serum fibrin-fibrinogen degradation products (FDP) were investigated. In 11 of the 24 patients, several instances of gastrointestinal bleeding due to esophageal varices rupture were documented and 5 patients died of unarrestable bleeding. In our study, we evaluated whether the cause of bleeding was the development of intravascular coagulation or the severity of hepatic failure. A statistically significant difference between F VIII:C, F VIIIR:AG/C ratio, and serum FDP was found in bleeding in comparison with non-bleeding patients. An inverse correlation between the F VIII:C plasma level and serum FDP as well as a direct correlation between F VIII AG/C ratio and serum FDP in the group of bleeding patients were also found. These data seem to suggest a hypercoagulable state which was more significant in the 5 patients who died owing to bleeding. Furthermore, only 1 of these patients had severe hepatic failure. From this study it appears that, in cirrhotic patients, bleeding is related more to the appearance of disseminated intravascular coagulation, as a consequence of both hemodynamic and endothelial changes, than to the degree of hepatic failure itself.
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PMID:Bleeding in cirrhotic patients: a precipitating factor due to intravascular coagulation or to hepatic failure? 641 23

We examined the intra- and postoperative behavior of antithrombin III (AT), factor V, VIII, and fibrinogen in 27 elective surgical patients without evidence of disseminated intravascular coagulation (DIC) and treated according to the concept of blood component therapy inaugurated at our hospital in 1975. The intraoperative depletions of AT and fibrinogen were proportional to the transfusion volumes and correlated significantly. AT, fibrinogen, and especially factor V and VIII were significantly mobilized during surgery. A greater intraoperative depletion of AT was significantly associated with a faster recovery during the first 24 postoperative h. The AT activity was virtually stable over a period of 4 weeks in CPD-adenine red cell concentrates; fresh frozen plasma and whole blood are thus not essential as a source of AT. The application of our concept did not increase the frequency of thromboembolic complications, despite the fact that the intraoperative AT values fell below the presumed 'critical' level of 60-70% in some patients. The probable reasons are the brief duration of such levels, the simultaneous depletion of coagulation-promoting plasma constituents (e.g. fibrinogen), and the use of antithrombotic prophylaxis. Our results suggest no reasons for a routine use of fresh frozen plasma in patients with a loss and replacement of less than about 75% of their blood volume.
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PMID:Antithrombin III and related parameters in surgical patients receiving blood components. 642 32

VIII:C, VIII:CAg, VIIIR:Ag and VIIIR:Cof were determined repeatedly in nine shock patients with suspected DIC and in five patients with uncomplicated acute myocardial infarction and compared with the clinical course and the severity of DIC as reflected by a score based on six routine coagulation and fibrinolysis parameters. All shock patients showed high levels of VIIIR:Ag, VIIIR:Cof, and VIII:CAg, averaging fivefold to sixfold the normal level, of VIII:C averaging threefold the normal level. VIIIR:Cof and VIIIR:Ag significantly correlated in both groups of patients. In shock patients, VIII:C values were lower than VIII:CAg and varied between 40-90% of VIII:CAg. There were significant negative correlations between the DIC score on the one hand and ratios of VIII:C/VIIIR:Ag, VIII:C/VIII:CAg, and VIII:CAg/VIIIR:Ag on the other. The two patients who died from irreversible shock had the highest DIC score and lowest ratios of VIII:C/VIIIR:Ag and VIII:CAg/VIIIR:Ag as well as VIII:C/VIIIR:Cof and VIII:CAg/VIIIR:Cof. Released VIIIR:Ag multimers possess the ristocetin cofactor activity. In DIC, VIII:CAg is partially proteolyzed, however, less than VIII:C. The quotient VIII:C/VIIIR:Cof or VIII:C/VIIIR:Ag is a good indicator of the severity of DIC and may have important prognostic value.
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PMID:Factor VIII (procoagulant activity VIII:C, and antigen VIII:CAg, related antigen VIIIR:Ag and ristocetin cofactor VIIIR:Cof) in intensive care patients with clinically suspected disseminated intravascular coagulation (DIC). 643 9

An experimental animal model of disseminated intravascular coagulation (DIC) induced by the co-infusion of coagulant-active phospholipid and activated Factor X (Factor Xa) is described. The infusion of Factor Xa at a dose of 6.6 X 10(-12) mol/kg with phosphatidylcholine/phosphatidylserine (PCPS) lipid vesicles at a dose of 4.0 X 10(-8) mol/kg was associated with significant falls in the levels of fibrinogen and Factors V and VIII, and a bleeding diathesis developed. Assays of Factors V and VIII were performed by a one-stage prothrombin time and activated partial thrombin time system, respectively. In additional experiments, the effect of the same dose combination of Factor Xa/PCPS on Factor V kinetics was studied by preinfusing 125I-labeled Factor V. After Factor Xa/PCPS infusion, Factors VIII and V were reduced at 2 min by 90 and 50% of the preinfusion levels, respectively, and at 1 h by 80 and 75%, respectively. During the same period, there was little change in the total circulating radioactivity. Autoradiography indicated small but detectable levels of circulating proteolytic products of Factor V that comigrated with peptides obtained by the incubation of Factor V with Factor Xa and activated protein C. The majority of radioactivity remained associated with the intact single-chain precursor Factor V. These observations suggested maintenance of the precursor pool after the onset of DIC. This was confirmed by performing two-stage assays of Factors V and VIII, whereby each was completely converted to the active cofactor, i.e., Va and VIII:Ca, by preincubation of the test sample with thrombin before assaying in a one-stage system as before. The Factor V levels assayed by the two-stage procedure did not change appreciably over 1 h. The Factor VIII levels fell but corrected within 1 h at a time when the level measured by a one-stage assay remained depressed. These results indicate that in the dog, infusion of Factor Xa/PCPS induces changes characteristic of DIC, and this is associated with the appearance of Factor V peptides characteristic of the expression of Factor Xa and activated protein C-like activities. The differences noted between the one-stage and two-stage assays suggest that the one-stage assay is measuring the activated fraction of each cofactor and not the total level of the available precursor for each activated species. The results suggest a close correlation between the activated fraction of both cofactors and the hemostatic abnormality that occurs in DIC.
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PMID:Studies of Factors V and VIII:C in an animal model of disseminated intravascular coagulation. 643 44

A 21 year old caucasian male, who was admitted to the medicine service for respiratory problems and hematemesis was ultimately diagnosed as having metastatic choriocarcinoma. Plasma samples were analyzed for prothrombin time (PT), activated partial thromboplastin time (APTT), platelets, and clot activation time for fibrinogen (FIB), and coagulation factors II, V, VII, VIII, X and XII. Abnormal clotting parameters included thrombocytopenia, PT, APTT, FIB, factors II, V, VII, and X. The coagulation abnormalities indicate the patient was in a state of consumption coagulopathy possibly induced by hepatic metastasis of the primary tumor.
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PMID:Abnormal hematological indices associated with metastatic choriocarcinoma in a young man. 657 23


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