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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two thirds of the patients with peripheral arterial occlusive disease have to be treated conservatively, for only up to 30% can be revascularized by operative methods. Using the pharmacological differential treatment the grade of compensation and localization of the obliterative process has to be considered. Ignoring the usual basic therapy (elimination of heart failure and pathological bradycardia, systemic walking-exercise, anticoagulation etc.) intrafemoral long-term application of energetic phosphate (i.e. nucleotid-nucleosid-mixtures) leads to a positive result in nearly two thirds (n = 97 legs) with a degree of II to IV of Fontaine. Whereas the snakes' encyme Ancrod with the effect of defibrination was successful in almost 70% of the patients with arterial insufficiency (n = 45) including the degree II B (painless walking-distance under 100 meters). Energetic phosphates, applied to the arteria femoralis, are most successful in degree II with claudication intermittens. Ancrod should be used respectively for patients with pain during rest. These results are discussed with respect to compensation and localization of arterial occlusive disease, acute and chronic measurements of the hemodynamics by use of Doppler ultrasound and strain gauge plethysmography and with respect to variation of the concentration of the metabolic parameters lactate and pyruvate--the latter when defibrination was performed.
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PMID:[Pharmacological treatment of chronic arterial occlusive disease (author's transl)]. 49 58

Two drugs, 2,6-cis-diphenylhexamethylcyclotetrasiloxane (Cisobitan) and estramustine-17-phosphate (Estracyt) were given to patients with poorly differentiated metastatic carcinoma of the prostate. The effect of the drugs on blood coagulation was investigated. Some parameters showed changes during the treatment: Antithrombin III decreased in the Estracyt treated patients to a level which might imply a thrombogenic effect. Fibrinogen decreased, whereas factor VIII showed no consistent change. Normotest changes appeared to correlate with liver damage whereas antithrombin III showed no change. Increased levels of fibrinogen degradation products and fibrinopeptide A (FPA) were more frequent in the group of deteriorating patients. However, the number of FPA analyses were too small for any definite conclusions regarding possible disseminated intravascular coagulation.
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PMID:Blood coagulation studies in patients with advanced carcinoma of the prostate treated with 2,6-cis-diphenylhexamethylcyclotetrasiloxane or estramustine-17-phosphate. 66 37

Anticoagulation largely prevents clotting and defibrination in extravascular blood pools. Systemic or local heparin may be more effective than local citrate phosphate dextrose in preventing coagulation in extravascular blood, if there is to be a lag period greater than 60 minutes between blood loss and collection. Nonanticoagulated extravascular blood in the thorax or peritoneal cavity is completely defibrinated within 20 minutes and is a potential risk in large autotransfusions. Blood in the thorax is better preserved than peritoneal blood after local or systemic heparinization.
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PMID:Blood surface interactions in extravascular salvageable blood pools. 89 77

Fibrinogen content was determined for each of 50 units of citrate-dextrose-phosphate (CPD)-preserved whole blood, packed red blood cells reconstituted with 250 ml. of saline, and packed red cells reconstituted with 250 ml. of purified plasma protein fraction (PPF). The total protein and albumin were measured, by electrophoresis, on each of 10 units of the three varieties of blood. The fibrinogen content of the two types of reconstituted cells was significantly lower than that of whole blood. Although the total protein/albumin content of whole blood and PPF-reconstituted red cells was similar, saline-reconstituted cells were markedly deficient in both total protein and albumin. Low fibrinogen and platelet levels subsequent to transfusion with reconstituted packed red cells can lead to an erroneous diagnosis of disseminated intravascular coagulation. Administration of large quantities of saline-reconstituted packed cells could be an etiologic factor in postoperative interstitial pulmonary edema.
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PMID:Fibrinogen and albumin deficiencies associated with packed red blood cell transfusions. 109 Feb 9

The intravenous infusion of calcium 2-amino ethanol phosphate was coincidental with cardiopulmonary arrest in a 53-year-old woman with a history of multiple sclerosis. Resuscitation was followed by massive hemolysis, renal failure, adult respiratory distress syndrome, shock liver, and disseminated intravascular coagulation. This agent, in use by at least one practitioner in West Germany for the treatment of inflammatory and autoimmune disorders is not FDA approved for use in the United States, nor is clinical investigation underway. It is currently thought to be in use by about 200 practitioners throughout this country as treatment for multiple sclerosis. It is apparently obtained in West Germany and brought illegally into the United States. This is the first known report of an adverse drug reaction associated with the use of this product.
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PMID:Cardiopulmonary arrest following an infusion of calcium 2-amino ethanol phosphate. 209 69

A rabbit endotoxic DIC model was preliminarily performed. The structures of lysosomes and mitochondria in liver cells were evidently destroyed as observed under electronic microscope, whereas those rabbits pretreated with Re Du Qing (RDQ, formerly named anti-inflammatory No. 6)--a mixture of Chinese traditional herbs providing antipyretic and detoxifying action, showed principally normal ultrastructure in liver cells. In lysosomal functional studies, the activity of the lysosomal marker enzyme--acid phosphate (ACP) was 79.0 +/- 4.7% (M +/- SD) in model group, higher than pretreated group (54.01 +/- 4.0%, P less than 0.01). Studies on the mitochondrial function showed that the significant criteria of the respiratory activity of mitochondria--respiratory control ratios (RCR) was 2.83 +/- 1.08 in model group and markedly lower than pretreated group (5.46 +/- 1.25, P less than 0.01). Mitochondrial ATPase activity (mu mol pi/min/mg pr.) was lower in model group (0.280 +/- 0.015) than in pretreated group (0.341 +/- 0.018, P less than 0.05). Lipid peroxide (LPO) in liver homogenates and serum were 1.86 +/- 0.43 n mol MDA/mg pr. and 12.26 +/- 0.84 n mol MDA/ml respectively in model group, whereas in pretreated group they gave a much lower value (1.19 +/- 0.12 and 6.55 +/- 2.97) respectively. Those data showed very significant difference between two groups (P less than 0.01). All of the above indices of pretreated group yielded values close to those of normal control group. The results of experimental study in vitro were identical to those of experimental study in vivo. These experimental studies suggested that RDQ provide antagonistic effect on endotoxin induced damage of lysosomes and mitochondria.
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PMID:[Experimental studies on the antagonistic effect of re du qing on endotoxin-induced damage of lysosomes and mitochondria]. 279 Nov 62

A series of 129 patients with closed injuries receiving more than 20 units (1 unit = 500 ml) of blood within the first 48 h of accident was analysed. The transfusion policy included type-specific crossmatched whole blood stored with citrate phosphate-adenine as the main replacement. One unit of fresh whole blood was transfused for every 5 to 6 units of stored blood. Also platelet concentrates and fresh frozen plasma were in routine use. The patients required 340 surgical procedures, on average 2.6 per patient. Thrombocytopenia with a lowest recorded platelet count of less than 100,000/mm3 occurred in 81 patients (63 per cent) of whom 18 had disseminated intravascular coagulation. This serious complication seemed to be associated with large retroperitoneal blood accumulations, the latter possibly acting as an enhancing factor. The mortality rate in the whole series was slightly lower than recorded previously in the literature. Among patients receiving 21 to 39 blood units the mortality was 25 per cent and among those receiving 40 units or more the mortality was 52 per cent.
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PMID:Outcome of closed injuries exceeding 20-unit blood transfusion need. 322 43

Concentrations of plasma fibrinopeptide A (FPA) were measured by radioimmunoassay in 50 patients with venous thromboembolism or disseminated intravascular coagulation or both. A consistent discrepancy was observed in values obtained with two anti-FPA antisera. Analysis of extracts from plasma of these patients by high-performance liquid chromatography (HPLC) revealed the presence of a phosphorylated and an unphosphorylated form of the A peptide. Differences in concentrations of FPA measured with the two antisera could be accounted for by their different reactivity with phosphorylated FPA (FPA-P). The differences were abolished by treatment with alkaline phosphatase. A good correlation was observed between the FPA-P content of free A-peptide material and of fibrinogen in plasma as determined by HPLC (r = .88, P less than .001, n = 11). In patients with elevated FPA levels, the mean FPA-P content of fibrinogen was significantly higher (P less than .002, n = 13) than in patients with normal FPA levels (n = 8) and in healthy controls (n = 14). Phosphorus in fibrinogen did not correlate with fibrinogen degradation products or fibrinogen levels and became normal on adequate anticoagulation. Therefore, blood-clotting activation may lead to a high phosphate content of fibrinogen and of free FPA in plasma.
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PMID:Fibrinopeptide A and the phosphate content of fibrinogen in venous thromboembolism and disseminated intravascular coagulation. 369 10

An enzyme-linked differential antibody immunosorbent assay has been developed for the quantification of alpha2-plasmin inhibitor-plasmin and alpha2-macroglobulin-plasmin complexes. In this method the inhibitor-plasmin complex is bound to a surface by an inhibitor-specific antibody, and the plasmin bound to the inhibitor is quantified by a second antibody, rabbit antiplasminogen F(ab')2, labeled with alkaline phosphatase. The hydrolysis of p-nitrophenyl phosphate by the alkaline phosphatase is expressed in femtomoles of plasminogen per milliliter, by reference to a standard plasminogen curve. Inhibitor-enzyme complexes were generated in plasma by the addition of plasmin or of urokinase. The concentration of plasmin added was well below the plasma concentration of alpha2-plasmin inhibitor (1 microM) or of alpha2-macroglobulin (3.5 microM), so that neither inhibitor would be fully saturated with enzyme. Under these conditions increasing amounts of plasmin generated an increase in both alpha2-plasmin inhibitor-plasmin and alpha2-macroglobulin-plasmin complexes. Varying amounts of plasmin were incubated with each of the purified inhibitors in the concentration found in plasma, and the complexes. Varying amounts of plasmin were incubated with each of the purified inhibitors in the concentration found in plasma, and the complexes that formed were quantified by immunoassay. These studies made it possible to quantify the distribution of plasmin between the two inhibitors in plasmin or urokinase-treated plasma. In plasmin-treated plasma, 10% or less of the plasmin bound to both inhibitors was in complex with alpha2-macroglobulin. In contrast, between 19 and 51% of the plasmin generated in urokinase-activated plasma was bound to alpha2-macroglobulin. Thus, major changes in the distribution of plasma were observed, according to whether plasmin was added to plasma or whether plasminogen was activated endogenously. The pattern of inhibitor plasmin complexes generated in vivo by the therapeutic infusion of urokinase was similar to that found for urokinase-activated plasma. 23 normal individuals had low levels of alpha2-plasmin inhibitor-plasmin complexes, whereas six patients with laboratory evidence for disseminated intravascular coagulation demonstrated a 16- to 35-fold increase in he concentration of these complexes. These data indicated that a useful new probe for the study of the fibrinolytic enzyme system had been developed.
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PMID:Alpha2-plasmin inhibitor and alpha2-macroglobulin-plasmin complexes in plasma. Quantitation by an enzyme-linked differential antibody immunosorbent assay. 616 34

Antithrombin III (AT III) is a plasma protein which acts as the principal inhibitor of thrombin and is a major modulator of intravascular coagulation. Hereditary deficiency of AT III leads to recurrent episodes of thromboembolism. Acquired deficiency of AT III occurs in persons with a variety of conditions, including severe liver disease and disseminated intravascular coagulation. Replacement of AT III may be important in some deficient persons. To determine if cryoprecipitate is a useful source of AT III, we measured the AT III content of cryoprecipitate prepared from citrate phosphate dextrose blood using coagulation and fluorogenic assays and immunoassays. Using the fluorogenic assay, we also determined the effect of adding heparin to blood on the cryoprecipitation of AT III. Functional and antigenic AT III levels were similar to those of normal plasma in all citrate phosphate dextrose blood units tested, indicating that AT III is not concentrated in cryoprecipitate. Heparin had no effect on the cryoprecipitation of AT III.
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PMID:The antithrombin III content of cryoprecipitate prepared from blood collected with and without heparin. 640 59


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