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)

A case report of a patient with primary fibrinolysis resulting in hemorrhage after an oral surgical procedure has been presented. A comparison was made between DIC and primary fibrinolysis in patients with carcinoma of the prostate gland; etiology, clinical findings, diagnosis, and treatment were discussed.
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PMID:Primary fibrinolysis after oral surgery. 16 85

The inhibitory effects of a newly synthesized protease inhibitor, Gabexate mesilate (FOY), on experimental disseminated intravascular coagulation were studied as compared with those of aprotinin or heparin. Thrombin, tissue thromboplastin, and endotoxin were used as DIC trigger substances. As parameters on DIC, platelet counts, white blood cell counts, neutrophilic leukocyte counts, fibrinogen, fibrin degradation products, platelet retention, platelet aggregation, prothrombin time, partial thromboplastin time were served. The drug efficacy in each parameter were expressed by the score system and analyzed statistically. The results were summarized as follows; (1) In thrombin-induced DIC, FOY was apparently superior to the other drugs (p less than 0.05). (2) In thromboplastin-induced DIC, heparin was slightly more effective than FOY or aprotinin. (3) In endotoxin infusion, there were no significant differences among them. In conclusion, the results of the present study suggest that FOY was more effective than heparin or aprotinin on experimental DIC.
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PMID:Inhibitory effects of gabexate mesilate (FOY) on experimental DIC. 22 8

The antitumor agents 5-(3,3-dimethyl-1-triazenyl)imidazole-4-carboxamide (DIC) and 5-[3,3-bis(2-chloroethyl)-1-triazenyl]imidazole-4-carboxamide (BIC) are substrates for NADPH-requiring microsomal enzymes of mouse liver. The products of DIC oxidation are 5-aminoimidazole-4-carboxamide (AIC) and formaldehyde. Those for BIC are AIC and, presumably, 2-chloroacetaldehyde. For DIC, the reaction has a pH optimum of 9.0; and the Michaelis constant (Km) is 0.25 mM. At lower pH values, the Km is not greatly increased; but there is a sharp rise in the Km values above pH 9.0. For the enzyme-catalyzed production of AIC from BIC, the pH optimum is 7.5; the Km value for BIC is 0.47 mM. Of a variety of tissues tested for enzymatic activity, only liver accomplishes the conversion of DIC and BIC to AIC. Most of the activity in the liver is located in the microsomal fraction, although detectable activity is present in washed mitochondria. For liver microsomes, the rate of reaction for BIC is greater than that for DIC, but apparently neither rate is fast enough to allow extensive metabolism of large doses of these agents.
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PMID:Microsomal metabolism of triazenylimidazoles. 24 85

Cold-insoluble globulin is normally present in plasma and serum at concentrations of 27.52 +/- 4.60 and 23.46 +/- 5.18 mg/dl, respectively (means +/- SD). The concentration of CIg in blood samples was significantly decreased in DIC syndromes (14.69 +/- 6.55 mg/dl; p less than 0.001). A strong, positive correlation was found with AT-III (r = 0.68) and a less striking one with Plg. Although alpha 2-PI was shown to be significantly decreased in DIC syndromes (p less than 0.001), a weak, inverse correlation was found between CIg and alpha 2-PI (r = -0.29). Immunologically cross-reactive substances were found to be widely distributed in association with the cells and tissues of mesenchymal origin, including fibroblasts, adipose cells, smooth muscle cells, and basement membranes. The glomerular basement membrane was an exception and is currently believed to be of different origin. In the kidney, fluorescence was found in the mesangium. Cold-insoluble globulin is also present as a component of cryofibrinogen that forms a solid gel at low temperatures. Sodium dodecyl sulfate polyacrylamide gel electrophoresis revealed that CIg in this fraction was rather homogeneous. Although closely migrating doublets were occasionally seen in the 440,000-dalton region on gels of unreduced samples, monomeric derivatives with a molecular weight of 220,000 or less, which have been claimed to occur in circulating plasma, were not observed. Thus, intact dimeric CIg appears to be the form of the molecule that complexes with fibrinogen. Cold-insoluble globulin is the fraction that was shown to exist as an independent entity from fibrinogen at an ambient temperature by immunoelectrophoresis and ultracentrifugation. However, very rapid formation of highly polymerized complexes in the sol phase at low temperatures was manifested by the finding of a sharp increase in light-scattering intensity using the technique of quasielastic light scattering. A control study on a mixture of normal CIg and fibrinogen disclosed no appreciable change in the temperature range between 37 and 8.5 degrees C. A comparative study on a mixture of cryofibrinogen-derived CIg and normal fibrinogen revealed an intermediate light-scattering pattern. After 2 hr at 8 degrees C, this mixture reached a state of equilibrium, where no further polymerization occurred. The secondary structures of normal and cryofibrinogen-derived CIg, determined by circular dichroism, showed no appreciable difference. A noteworthy finding was the almost complete absence of alpha-helices and a relatively high proportion of beta-structure in both forms of CIg. Amino termini of the fibrinogen moiety of cryofibrinogen were found to consist of alanine, tyrosine, and a small quantity of aspartic acid, consistent with the NH2 terminal moiety composition of normal fibrinogen but not of soluble fibrin monomer complex.
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PMID:Distribution of cold-insoluble globulin in plasma and tissues. 29 82

A 3-year-old boy with partial No. 9 tetrasomy is described. The patient showed markedly retarded physical and mental development as well as multiple congenital anomalies. Routine chromosome analysis revealed an extra C-group chromosome. It had a pronounced secondary constriction at the proximal part of its long arm. Based on studies by a variety of banding techniques, the extra chromosome was identified to be an iso-dicentric No. 9 chromosome with inactivation of one of the two centromeres, the karyotype being 47,XY, + DIC (9)(Q2101). The value of BrdUrd treatment was emphasized in the detection of a very small piece of euchromatin within a long stretch of constitutive heterochromatin.
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PMID:Partial tetrasomy 9(9pter to 9q2101) due to an extra iso-dicentric chromosome. 30 83

The evidence for intravascular coagulation in liver diseases is critically reviewed. Alternative mechanisms for hypofibrinogenemia and the accelerated disappearance of fibrinogen from blood are proposed, such as loss into extravascular compartments (e.g., ascites, areas of liver necrosis, etc.). Possible mechanisms other than DIC for the elevation of serum FDP are also considered, such as extravascular fibrinogen proteolysis with subsequent transfer of FDP to blood. Therapy is discussed with reference to the current knowledge on pathophysiology of the coagulation defect in liver diseases.
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PMID:Diffuse intravascular coagulation in liver disease? 33 13

The newborn infant, particularly when premature, has a haemostatic mechanism which may not be entirely capable of withstanding the onslaughts of trauma, infection, asphyxia or other complications of the neonatal period. He is at risk of local or diffuse haemorrhage, which may at times be serious or even life-threatening. The cause of haemorrhage during the newborn period can generally be ascertained by a careful history and brief physical examination directed toward recognition of any predisposing factors or underlying diseases. Screening laboratory tests can usually be correctly interpreted as long as certain laboratory artifacts and physiological peculiarities of the neonatal coagulation mechanism are kept in mind. Diagnosis of and therapy for vitamin K deficiency and haemophilia in the healthy-appearing neonate is generally carried out with little difficulty. The seriously ill neonate with bacterial sepsis, respiratory distress syndrome, or extreme immaturity presents greater problems, for laboratory tests may be more difficult to obtain and interpret and underlying conditions may be untreatable. DIC occurs commonly in such neonates, and transfusion therapy, with or without heparin, is often unsuccessful. A persistent dilemma are those neonates with fatal intravascular haemorrhage, in whom definable haemostatic abnormalities are few and transfusion therapy is futile.
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PMID:Neonatal coagulation: normal physiology and pathophysiology. 35 Apr 67

A patient with cerebral malaria complicated by full-blown DIC, after failing to respond to other forms of treatment, was successfully treated by exchange transfusion. To the best of the authors' knowledge, this may be first reported case of full-blown DIC in malaria successfully treated by exchange transfusion.
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PMID:Exchange transfusion in cerebral malaria complicated by disseminated intravascular coagulation. 39 Jul 23

The concentrations of plasmatic fibrinogen and its degradation products (FDPs), and the paracoagulation test using serial dilution of protamine sulphate (SDPS) were determined during the third trimester of pregnancy, labor, and puerperium. Singificant increases in the concentrations of fibrinogen and FDPs were observed throughout the process of pregnancy and birth, combined with both positive and negative SDPS tests. We suggest that these findings do not indicate a process of physiological DIC.
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PMID:Is there a physiological intravascular coagulation in obstetrical cases? 41 51

We conclude that DIC can occur as a result of sickle cell crisis in the absence of sepsis and we recommend that patients with sickle cell disease, particularly those with hemoglobin SC disease, presenting in crisis should be considered at risk for the development of disseminated intravascular coagulation. With symptomatic treatment and improvement of the crisis, our patient's coagulopathy resolved.
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PMID:Disseminated intravascular coagulation in sickle cell crisis. 43


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