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)

During pregnancy, 12 women who smoked more than 10 cigarettes/day and 12 nonsmokers had blood taken and analyzed at 12, 20, 25, 30, 34, and 38 weeks of gestation. Fibrinogen, plasminogen, plasminogen activator, serum fibrin degradation products, antithrombin 3, alpha 1 antitrypsin, and alpha 2 macroglobulin were measured. The only significant (p .05) difference was that plasma fibrinogen was lower among smokers at 20 weeks. However, there were other patterns of difference -- mean fibrinogen and plasminogen levels were slightly lower throughout pregnancy and reached a lower peak in the smoking group. Fibrinolytic activity fell in the smokers to the same low level as in nonsmokers by 38 weeks, but at a slower rate. Serum fibrin degradation products and alpha 2 macroglobulin were consistently higher in the smoking group. Although the findings showed no major disseminated intravascular coagulation in smokers, there was a pattern of a possible low-grade syndrome.
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PMID:The influence of smoking on the haemostatic mechanism in pregnancy. 6 96

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

Endotoxin from E. coli was infused into the distally ligated common bile duct of rabbits under the static pressure of 25 cm H2O. Fibrinogen, soluble fibrin monomer complexes, antithrombin III, leukocyte and platelet counts were estimated before, and 2, 4, and 6 h after endotoxin infusion. All parameters were found significantly changed 2 h after endotoxin infusion. While fibrinogen level, AT III, leukocyte and platelet counts decreased after the endotoxin infusion the amount of SFMC increased. The change of hematological parameters showed a pattern characteristic of disseminated intravascular coagulation (DIC). In accordance with this microclots in the glomeruli of the kidneys could be demonstrated in all endotoxin-treated animals by pathological study. The findings suggest that by endotoxin infusion into the common bile duct, as a focal origin, DIC can be produced.
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PMID:[Disseminated intravascular coagulation (DIC) after endotoxin infusion into the common bile duct of rabbits (author's transl)]. 38 87

With the use of cohort labeling with 75Se-selenomethionine, simultaneous platelet, fibrinogen, and plasminogen survival studies were carried out in 8 patients with chronic alcoholic liver disease and in 5 normal subjects. Clinical features, liver function tests, coagulation and fibrinolytic system activities, and platelet function were also assessed. On the basis of platelet survival, the patients could be divided into two groups. Three patients had shortened platelet survival; they were all thrombocytopenic and had greater prolongation of the prothrombin time (PT) and activated partial thromboplastin time (PTT) than the other 5 patients. However, platelet turnover was decreased in all the patients, and there was no difference between the two groups with regard to fibrinogen or plasminogen survival nor in the in vitro evidence of disseminated intravascular coagulation (DIC). Fibrinogen survival was increased in 5 of the 8 patients. Plasminogen survival was normal in 6 patients and prolonged in 2 patients with very low plasminogen levels. The absence of increased fibrinogen turnover in the patients studied indicates that the abnormalities in coagulation tests were not due to consumption coagulopathy. The authors' studies suggest that, at least for patients with chronic stable alcoholic liver disease, the concept that the coagulopathy of liver disease is due to increased utilization of clotting factors should be revised with caution.
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PMID:The hemostatic defect of chronic liver disease. Kinetic studies using 75Se-selenomethionine. 42 8

Twenty-seven patients requiring massive transfusions were studied prospectively to determine whether administration of stored, modified whole blood induced a primary disorder of hemostasis evidenced by generalized microvascular oozing. Platelet counts fell in proportion to the number of units of blood transfused. In contrast, the levels of factors V and VIII correlated poorly with the units of blood transfused, 85% of the total variation in the levels being due to influences other than transfused blood. Levels of all other clotting factors were unrelated to the number of units of blood given. Eight patients developed abnormal bleeding. The cause appeared to be dilutional thrombocytopenia in five patients, and DIC in three. In six of the eight, bleeding was controlled with platelet concentrates alone. Two patients were given cryoprecipitate also. The most useful laboratory test for predicting abnormal bleeding was the platelet count. Fibrinogen levels should be followed as an aid in the diagnosis of DIC. The BT, PT, and PTT were not helpful in assessing the cause of bleeding, unless they were greater than 1.5 times the control value. We recommend that any patient receiving massive transfusions who develops diffuse microvascular bleeding be given platelet concentrates. Platelet counts as high as 100,000 may be required to control bleeding from surgical wounds. It is not necessary to supplement transfusions of stored, modified whole blood with fresh blood or fresh frozen plasma.
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PMID:Hemostasis in massively transfused trauma patients. 46 85

Sepsis of the newborn induced by gram negative bacteria, especially E. coli is often accompanied by a severe coagulation disorder. It can be treated by blood exchange transfusion (ET) with heparinized blood. In this study the hematological effect obtained by the exchange transfusion was investigated in rabbits after induction of a generalized Shwartzman reaction by two spaced injections of endotoxin (75 microgram/kg) 24 hrs. apart. Three groups of 6 animals each were investigated: group I: without endotoxin but with ET (controls); group II: endotoxin without ET; group III: endotoxin with ET. Fibrinogen, soluble fibrin monomer complexes (SFMC), fibrin(ogen) degradation products (FDP), platelet- and leukocyte counts and urine volume (ml/hr) were estimated. In group II a decline in the fibrinogen level, and in platelet and leukocyte count, as well as an increase in SFMC and FDP could be observed from 6 hrs. on after the second endotoxin injection. In group III 6 hrs. after the second endotoxin injection, exchange transfusion with heparinized blood was performed. Variance analysis showed significant differences in all parameters, except in the urine volumes after exchange transfusion between group III and group II. By exchange transfusion an approach of the values towards the values of the controls could be recognized. The findings indicate, that by blood exchange transfusion the hematological consequences of the endotoxin induced DIC can be corrected, while the dysfunction of the kidneys can be improved only slightly.
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PMID:The effect of heparinized blood exchange transfusion on endotoxin induced disseminated intravascular coagulation (DIC). 50 9

Platelet number, spontaneous aggregation, ADP- and adrenaline-induced aggregation, fibrinogen, and factors 2, 5, 7, and 10, were investigated in a series of 40 consecutive patients admitted to the clinic following severe head injury. Data were evaluated daily during the first week after trauma. Platelets were significantly decreased, particularly in non-survivors; there was no pathological spontaneous aggregation, except in a group of 22.5% of cases who had a mean age of 23.5 years. ADP-induced aggregation was negative in 69% of cases, and adrenaline-induced aggregation was absent in only two non-survivors. Fibrinogen was markedly reduced during the first five days, thereafter normalizing or increasing towards the end of the week. The other investigated values remained within their normal range of 70--130%. The results give no evidence of disseminated intravascular coagulation as a generalized and frequent phenomenon in severely head injured patients. There are, however, signs of latent consumption coagulopathy, which support data from the literature that indicate focal microthrombosis in contused brain areas.
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PMID:Disturbances of the coagulatory system in patients with severe cerebral trauma II. Platelet function. 51 79

Fibrinogen-fibrin-related antigen (FR antigen) was isolated from as little as 1 ml of human plasma by immuno-affinity chromatography with agarose-bound antibody to human fibrinogen. N-terminal analysis was performed to determine the nature and extent of proteolytic degradation of the FR antigen in patients with disseminated intravascular coagulation and in normal subjects. Thrombin cleavage of the A- and B-peptides from fibrinogen in vitro was monitored by the appearance of N-terminal glycine, and an increase in glycine was shown in the FR antigen of patients with disseminated intravascular coagulation. As plasmin progressively degraded fibrinogen, increases in N-terminal alanine, aspartic acid and lysine were observed, corresponding to the known plasmin-cleavage points of fibrinogen; increases in these N-terminal amino acids were also found in the patients' FR antigen. Thrombin treatment in vitro was used to remove fibrinopeptide A (N-terminal alanine) from the samples and to reflect specifically the N-terminal alanine at the plasmin-cleavage point (Arg-42-Ala-43) of the B beta-chain on assay; this alanine was increased progressively in the FR antigen of a patient during urokinase therapy, and was high in other patients when the FR antigen was examined by this procedure.
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PMID:Quantitative N-terminal analysis of fibrinogen-fibrin-related antigen [FR antigen] from human plasma. 54 36

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

This is an investigation into thromboplastin time, partial thromboplastin time, plasma thrombin time, fibrinogen, and platelets in 30 patients with severe brain injury over 7--14 days. Platelets showed a very marked initial decrease and a slow return to normal around the seventh day. Fibrinogen was initially lowered in most of the cases, and raised from the second day onward. Changes in the other laboratory values were less definite. Latent signs of consumption coagulopathy were not accompanied by bleeding disorders, or by disseminated intravascular coagulation at autopsy. The severity of laboratory value changes clearly correlated with the extent of brain damage, and was significantly higher when the patient did not survive the first week after injury.
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PMID:Disturbances of the coagulatory system in patients with severe cerebral trauma. I. 70 71


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