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 effect of seven different anabolic steroids (Ethyloestrenol, Methenolone acetate, Norethandrolone, Methylandrostenediol, Oxymetholone, Methandienone, and Stanozolol) on three alpha-globulin antiprotease inhibitors of thrombin and plasmin was studied in men with ischaemic heart disease. In distinct contrast to the oral contraceptives, five of the six 17-alpha-alkylated anabolic steroids studied produced increased plasma Antithrombin III levels and five produced decreased levels of plasma alpha2-macroglobulin. The effect on plasma alpha1-antitrypsin levels was less clear-cut but three of the steroids examined produced significantly elevated levels. The increased plasma fibrinolytic activity which the 17-alpha-alkylated anabolic steroids induce is therefore unlikely to be secondary to disseminated intravascular coagulation.
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PMID:Effect of anabolic steroids on plasma antithrombin III. alpha2 macroglobulin and alpha1 antitrypsin levels. 5 96

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91

In 27 multiple trauma patients receiving standard shock management and intensive care, coagulation and fibrinolysis were investigated after early heparinization. The general coagulation tests did not imply any impaired clotting function. Platelets and factors I, II, and V decreased without induction of hypocoagulability. There was considerable decrease in plasminogen, whereas FDP ranged within normal; thus, a hyperplasminemia can be excluded. Antithrombin III remained within normal range; even in nonsurvivors there was no depletion, although their antithrombin III activity was significantly lower. In comparison to 50 trauma patients - a comparable group with regard to trauma patterns, shock management, and intensive care - there were no significant differences in volume requirements or mortality rate. Whether early heparinization is effective in preventing disseminated intravascular coagulation (DIC) related organ failure remains to be seen.
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PMID:Coagulation and fibrinolysis in multiple trauma after early heparinizing. 26 99

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.
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PMID:Endotoxin-induced intravascular coagulation (DIC) and its therapy. 40 May 81

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

Part I: Immunological assays of clotting factors in the diagnosis of liver diseases. The immunological determination of Antithrombin III is a good measure of the capacity of the liver to synthesize plasma proteins. Antithrombin III concentration in serum correlated significantly with the prothrombin time and the activity of cholinesterase. The immunological determination of factor VIII related antigen seems to be important for the early recognition of the transition of an acute hepatitis into a chronic course. While following uncomplicated acute hepatitis the level of factor VIII related antigen is normal after 40 weeks, it remains high in cases which become chronic. Immunological assay of factor XIII seems to be not very useful in the diagnosis of liver diseases. Part II: Management of coagulation disturbances in liver diseases. Except cases of hepatic coma the hemostatic abnormalities in chronic liver diseases are rarely severe enough that correction is necessary. Prothrombin concentrates are considered by most of the discussants as unnecessary and potentially dangerous. Transfusion of platelets is only neccessary when the platelet count is below 40.000 and surgery is planned. It is uncertain whether patients with chronical liver disease and laboratory signs of DIC benefit from heparin therapy. Although laboratory tests may be improved, prognosis, especially in cases of acute oesophageal bleeding, seems to be not changed by this treatment.
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PMID:[Summary of work session 1: Blood coagulation in gastroenterology]. 78 39

Consumption coagulopathy in childhood is still a serious problem. Besides treatment of the underlying diseases therapy of consumption coagulopathy was performed with heparin and nowadays with substitution of coagulation factors, especially antithrombin III concentrate, alone or in combination with heparin. We performed administration of AT III concentrates only, without additional heparin treatment in children with proven septicaemia (preterm infants n = 21, children beyond the newborn period n = 18). Antithrombin III, platelet count, fibrinogen, PT, aPTT and TT were assayed. These coagulation parameters turned to be normal 48 hours after normalisation of the antithrombin III plasma level-AT III increased to normal values within 24 hours after the initial substitution in all children. Lethal outcome was not observed after sole administration of AT III as well as no other side effects have been seen. In summary, these data indicate that consumption coagulopathy in childhood can be managed successfully with early substitution of AT III concentrate.
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PMID:[Treatment of disseminated intravascular coagulation with antithrombin III concentrate in children with verified infection]. 161 77

Fifty seven patients with schistosomiasis of the liver and spleen in both the compensated and decompensated states and 15 non-bilharzial subjects were studied. Fibrinogen, plasminogen, fibrinogen/fibrin degradation products, alpha 2-macroglobulin, antithrombin III and Cl-activator concentrations were evaluated in an attempt to assess abnormalities at various stages of the disease. The results showed a progressive decrease in fibrinogen and plasminogen concentrations; fibrin degradation products showed a progressive increase as the disease progressed. Together with a falling platelet count, these data indicate the possible occurrence of disseminated intravascular coagulation with enhanced fibrinolysis which was most pronounced in those who vomited blood. Antithrombin III concentration showed a progressive decrease in parallel with the progress of the disease, possibly due to decreased synthesis or increased consumption, or both. Cl-activator concentration showed no significant change from that in normal controls at any stage of the disease. These findings provide further evidence that disseminated intravascular coagulation and enhanced fibrinolysis in the late stages of schistosomiasis may contribute to the haemorrhagic diathesis seen in the liver and spleen.
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PMID:Fibrinolysis and the bleeding tendency in patients with hepatosplenic schistosomiasis. 169 89

Together with a detailed presentation of the physiological role of antithrombin III and a description of the pathological states in which it's acquired deficiency requires substitutional therapy with an antithrombin preparation, this report contains the results of a clinical trial of such a preparation which is in use under the name of Kybernin. Patients with severe diseases and traumas, of a septic nature mostly, were included in the trial. The experimental group includes 20 such patients treated with Kybernin, and the control group had 12 patients who did not receive this preparation. The level of antithrombin III at the time of entering the study was an average of 40.1% in the experimental group, and 53.2% in the control group. The mortality of the treated group was 45%, and in the control group it was 66.7%. Clinical and laboratory results point to a favorable effect of Kybernin therapy in the suppression of disseminated intravascular coagulation.
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PMID:[Clinical study of the therapeutic value of Kybernin in the treatment of antithrombin III deficiency]. 180 88

In 69 children with severe infectious purpura (SIP), anomalies of hemostasis on admission were studied retrospectively. Forty-four children presented with disseminated intravascular coagulation (DIC) and 18 with factor VII deficiency +/- thrombocytopenia +/- antithrombin III deficiency. Seven patients were free of hemostasis anomalies. In 5 children, purpura was necrotic on admission, whereas in 9 additional patients skin necrosis occurred subsequently (5 patients with and 4 without DIC). Among the 18 children (26%) who died, 16 were in the DIC group. Factors II and V, fibrinogen and platelet counts were lower in children who died and were correlated with the prognostic score. In the DIC group, however, factor VII + X level was not correlated with the prognostic score and was equally low in fatal and non-fatal cases. Antithrombin III level was markedly decreased in patients who subsequently developed necrosis. These results indicate that factor VII level decreases early in the course of SIP and that consumption of physiologic coagulation inhibitors probably plays a central part in the development of necrotic purpura.
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PMID:[Hemostasis anomalies and prognosis during severe infectious purpura in children. Retrospective study in 69 cases]. 195 1


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