Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial thromboplastin time, thromboplastin time, plasma thrombin time, fibrinogen, thrombin-coagulase and reptilase times as well as platelet count. Normal values of these laboratory parameters were established for healthy newborns 1--5 days of age, and for healthy adults. It is suggested that especially partial thromboplastin time, the thrombin-coagulase and reptilase times, the latter influenced by fibrinolysis cleavage products, are representative for the tentative diagnosis of disseminated intravascular coagulation with fibrinolysis syndrome (DICFS). The platelet fall often lags 1--2 days behind the event. Moreover normal values for newborns, are markedly higher than those for older children or adults. In the presence of DICFS, a low-dose heparin therapy is immediately initiated. If completed defibrination is manifest, therapy is supplemented with urokinase and streptokinase, For DICFS with congenital sepsis, an exchange transfusion with heparinized fresh blood is the treatment of choice.
 ...
PMID:[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)]. 32 24

Thrombin or factor Xa added to plasma are inactivated by antithrombin III (At-III). The inactivation is accelerated by heparin, permitting assay systems which rapidly measure the At-III content of diluted plasma. Without heparin, the slow inactivation rates may be measured. Existing activity assays (fibrinogen or chromogenic substrates) and immunoassays of At-III have been reviewed. Correlation studies show a close correlation between the results of immunoassay and the results of most activity assays. In health, a narrow range of At-III has been found. The level is low in infancy. Fertile women have on the average somewhat lower levels than men. In old age, the level tends to drop. In clinical material studied with amidolytic assays, subnormal At-III levels were found in hereditary deficiency, liver disease, disseminated intravascular coagulation and in some cases with acute thrombosis. The amidolytic assays are rapid to perform, do not require experience in clotting technique and seem preferable in clinical routine work.
 ...
PMID:Antithrombin III: critical review of assay methods. Significance of variations in health and disease. 35 Jul 29

Acute promyelocytic leukemia (APL) is characterized by proliferation of morphologically abnormal promyelocytes and a severe bleeding diathesis. The abnormal promyelocyte is characterized by abundant, large granules, many of which are spindle-shaped. Electron microscopic appearance of the granules closely resembles that of Auer rods. The granules appear to possess tissue thromboplastin activity by both immunologic and clotting assays. Coagulation studies in APL are generally consistent with disseminated intravascular coagulation. Prolongation of the prothrombin time and elevation of fibrinogen degradation products are the tests that are most commonly abnormal. Although occasional reports indicate a favorable response of the coagulopathy to drugs that inhibit fibrinolysis, the use of prophylactic heparin appears to be the treatment of choice. The response rate of APL to chemotherapy regimens that contain an anthracycline is comparable to that of acute myelogenous leukemia. The recent description of the 15;17 chromosomal translocation which may be pathognomonic for APL is only the second example of a chromosomal marker of human neoplasia. Marked elevation of serum vitamin B12 and B12 binding proteins appears to be another characteristic feature of APL. An in vitro cell line of APL cells has been demonstrated to have the capacity to differentiate to functional polymorphonuclear leukocytes, but the cause for the maturation arrest is unknown.
 ...
PMID:Acute promyelocytic leukemia. 39 71

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.
 ...
PMID:The hemostatic defect of chronic liver disease. Kinetic studies using 75Se-selenomethionine. 42 8

Strenuous physical exercise leads to a significant shortening of blood clotting in various test systems. Such short times are also characteristic of those observed in sedentary patients with thrombosis or disseminated intravascular coagulation, and of those observed in experimental animals after thrombin infusion. The patients exhibit an increase in circulating fibrinopeptide A, which is attributed to thrombin action on circulating fibrinogen, and to an increase of fibrinogen degradation products, which is thought to indicate reactive fibrinolysis. To check whether physical exercise leads to fibrinemia, 10 healthy male volunteers were subjected to strenuous exercise on a bicycle ergometer. Blood samples were taken immediately before and on completion of the exercise period. Despite a significant shortening of the activated partial thromboplastin time, the thrombin time, and the Reptilase time, no increase of fibrinopeptide A could be demonstrated and the ethanol gelation test remained consistently negative. Simultaneously, the euglobulin lysis time was significantly shortened, whereas the fibrin(ogen) degradation products did not increase. The results indicate that the shortening of the coagulation times associated with physical exercise must be explained by mechanisms other than thrombin-mediated conversion of fibrinogen to fibrin.
 ...
PMID:Lack of fibrin formation in exercise-induced activation of coagulation. 43 23

An analysis of seven sporadic cases of Legionnaires' disease confirmed clinical features recorded during epidemics and identified aspects of the illness either unreported or not emphasized. Four patients had central nervous system abnormalities. Mental status changes included somnolence, obtundation, delirium, disorientation, and confusion. Three patients experienced visual hallucinations, and one patient without pneumonia had a grand mal seizure with residual memory deficit. Two patients had disseminated intravascular coagulation with thrombocytopenia, elevated split fibrin products, and prolonged partial thromboplastin and prothrombin times. Four patients had severe hypoxia; one patient had an exudative pleuritis. One patient whose treatment included erythromycin had radiologic improvement of his pneumonia despite deteriorating ventilatory function that led to death. The concept of Legionnaires' disease as a severe, diagnostically perplexing pneumonic illness is valid but too narrow. The emerging spectrum is that of a multisystem disease that, besides the lungs, often involves the central nervous system and can be accompanied by disseminated intravascular coagulation.
 ...
PMID:Sporadic cases of Legionnaires' disease: the expanding clinical spectrum. 43 28

The release of tissue thromboplastin after a severe brain injury can lead to a consumption coagulopathy. In a group of 83 patients with severe brain injury, platelet count, fibrinogen, prothrombin, partial thromboplastin time and thrombin time were investigated. The pathological laboratory findings in 14 were compatible with a consumption coagulopathy. These alterations were demonstrated during the first hours following trauma and represented an extra handicap for the patients who had to be treated surgically.
 ...
PMID:[Secondary blood coagulation disturbances after severe head injuries (author's transl)]. 44 May 17

Blood coagulation studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.
 ...
PMID:The pathogenesis of Trypanosoma congolense infection in calves. IV. The kinetics of blood coagulation. 44 53

Disseminated intravascular coagulation was induced in dogs by infusion of tissue thrombokinase. Its course was followed by coagulation tests, determination of the rate of microthrombosis, and measurement of organ functions and oxygen consumption. The therapeutic result of streptokinase administration at an early stage of pathological changes is demonstrated by improvement of the disturbed organ functions and oxygen supply as well as by the decrease in plasma-haemoglobin level. When streptokinase was administered at an advanced stage of organ damages, they remained irreversible, although repatency of the microvasculature had been reached.
 ...
PMID:[Experimental therapy of disseminated intravascular coagulation by streptokinase administration]. 51

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.
 ...
PMID:Oxygen-induced consumptive coagulopathy and its enhancement by lead acetate. 57 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>