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

Studies of coagulation hemostasis in 108 patients with rheumatoid arthritis have revealed that high blood coagulation is characteristic of this disease, and a number of coagulation parameters (antithrombin III, fibrinogen, fibrinolytic activity, ethanol test) point to intravascular microthrombi formation (disseminated intravascular coagulation). Along with hemostasis investigations, Willebrand's factor levels were measured in the blood plasma of 44 patients. Enhancement of the inflammatory process activity was found to be associated with elevation of this factor level and augmentation of the blood coagulation activity. These results permit considering Willebrand's factor as one of the diagnostic criteria of thrombophilic conditions in patients with rheumatoid arthritis.
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PMID:[The Willebrand factor in the diagnosis of hemostatic disorders in patients with rheumatoid arthritis]. 171 Jul 21

The pathophysiology of peripheral circulatory disturbance in patients presenting with vibration syndrome was studied from the viewpoint of blood coagulation. Plasma levels of fibronectin (FN), vitronectin (VN), thrombin-antithrombin III complex (TAT), and alpha 2-plasmin inhibitor-plasmin complex (PIC) were measured in 23 subjects who showed no evidence of vibration-induced white finger [VWF(-) group] and in 24 patients who presented with VWF [VWF(+) group]. In the VWF(-) group, plasma FN concentrations were elevated but plasma TAT and PIC levels were within the normal ranges. In the VWF(+) group, plasma FN concentrations were normal but plasma TAT and PIC levels were significantly elevated. In both groups, plasma VN concentrations were similar to those in normal controls. For purposes of comparison, 32 patients presenting with diabetes mellitus were also studied. They were divided into 2 groups, 13 subjects who showed no evidence of angiopathy [complication(-) group] and 19 patients who presented with angiopathy [complication(+) group]. In the complication(+) group, plasma TAT and PIC concentrations were significantly elevated, as in the VWF(+) group. These results suggest that in vibration syndrome, vibration, cold stimulus, or other factors first injure the vascular endothelium, resulting in a rise in plasma FN, and that in the VWF(+) group, augmentation of coagulation and fibrinolysis induces a state of compensated disseminated intravascular coagulation (DIC).
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PMID:Activation of blood coagulation and fibrinolysis in vibration syndrome. 172 Jul 65

We investigated changes in the concentrations of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2 plasmin inhibitor complex (PIC) after the intravenous administration of 4000 units of antithrombin III (AT III) concentrate to patients with fulminant hepatic failure (FHF), subacute hepatitis (SH), or liver cirrhosis (LC). FHF patients showed shortening of the initial half-life of exogenous AT III. In addition, a marked rise in plasma TAT was noted 3 to 6 h after the intravenous administration of AT III, even in patients who had a normal plasma TAT level before AT III therapy. In contrast, SH and LC patients showed no marked changes of plasma TAT levels after AT III administration. No marked changes were observed in the PIC concentration in any of the patients. These findings suggest that thrombin formation is increased in FHF and that simple measurement of the plasma TAT concentration is not an adequate method for assessing thrombin formation in FHF patients who have suspected disseminated intravascular coagulation associated with an apparent decrease in AT III synthesis. Instead, it seems necessary to measure the plasma TAT concentration in FHF patients after replacement therapy with AT III concentrate has been performed, to evaluate their hypercoagulability more accurately.
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PMID:Importance of measuring plasma thrombin-antithrombin III complex levels when using antithrombin III concentrate therapy in fulminant hepatic failure. 175 55

Blood rheologic properties and homeostasis system were comprehensively examined in 23 patients with fibrous-cavernous pulmonary tuberculosis and 58 patients with various chronic nonspecific pulmonary diseases complicated by respiratory failure. The patients were found to have signs of erythrocyte edema, their more rapid depletion, lower resistance and higher aggregation which was accompanied by increased hematocrit and normal erythrocyte count. The thromboelastograms showed that all all phases of blood coagulation were shortened and fibrinolysis was deeply depressed. There was an increase in activated partial thromboplastin and thrombin time, a reduction in the values of the prothrombin indices and antithrombin III activity and higher heparin levels. The fibrinogen level was either normal or reduced despite an increase in other acute phase reactants, followed by the appearance of large amounts of blocked fibrinogen in the blood. Analysis of the findings enabled one to regard a combination of the above changes as signs of the latent DIC syndrome. Determination of fibrin and fibrinogen degradation products in a deep and long-term inhibition of fibrinolysis loses its diagnostic significance.
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PMID:[Status of the hemostatic system in patients with chronic lung diseases]. 175 60

Platelet studies (total number and platelet aggregation) and coagulation assays (fibrinogen, factor VIII, and anti-thrombin III) were performed on systemic arterial blood of four control and four experimental adult cats that sustained a penetrating missile injury to the brain. Among the brain-wounded, a significant decrease in the total number of platelets and aggregates occurred 120 minutes after injury. Fibrinogen levels decreased significantly in the brain-wounded animals by 240 minutes after injury and continued declining until the end of the 6-hour experiment. No significant changes occurred in factor VIII and antithrombin III levels in wounded as compared with control animals. These results indicate that blood coagulation factors are altered following a missile wound to the brain. These alterations may, occasionally, lead to clinically manifested bleeding disorders, specifically disseminated intravascular coagulation. Thus, early analysis and control of the coagulation system in the brain-wounded patient should be considered to prevent and treat bleeding disorders in the setting of penetrating head injury.
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PMID:Coagulation changes after an experimental missile wound to the brain in the cat. 175 83

Thrombin-antithrombin III complex (TAT) concentration was measured in 27 control and 155 intensive care patients to (a) establish normal reference ranges, (b) measure thrombin generation in critically ill patients, and (c) determine the characteristics of the TAT assay for the diagnosis of disseminated intravascular coagulation (DIC) in children. The normal reference range was 1-4.3 micrograms/l (median 2.3 micrograms/l), and 89.7% of patients had raised TAT concentrations. Median TAT concentrations in the presence of DIC (27 micrograms/l) were significantly higher than in its absence (8 micrograms/l). Sensitivity, specificity, and positive and negative predictive values of the assay were 97.3%, 28.3%, 76.3%, and 81.3%, respectively, at a cut off of 4 micrograms/l. Excess thrombin production occurs in the majority of critically ill children. The TAT assay is potentially useful in the diagnosis of DIC in children.
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PMID:Enhanced thrombin generation in patients receiving intensive care. 177 88

In order to evaluate precisely the fibrinolytic states in clinical disorders, plasma levels of D dimer (cross-linked fibrin degradation products) were measured by a newly developed, rapid quantitative method based on the latex photometric immunoassay in patients with hematological malignancies, diabetes mellitus, collagen disease, liver disease, thrombotic disease and disseminated intravascular coagulation (DIC). Plasma levels of D dimer were elevated in a variety of diseases, especially in DIC. Patients with hematological malignancies, liver disease and thrombotic disease also had relatively high levels of D dimer. On the whole, D dimer values were positively correlated with plasmin-alpha 2-plasmin inhibitor complex and thrombin-antithrombin III complex. In addition, plasma D dimer was measured during fibrinolytic therapy with urokinase or tissue-type plasminogen activator; its elevation was detected in some patients. These findings indicate that accelerated fibrinolysis is frequently observed in a variety of diseases, and that a rapid quantitative measurement of D dimer would be valuable for the precise assessment of fibrinolysis in these disease states.
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PMID:[Evaluation of clinical usefulness of a rapid quantitative measurement of D dimer (cross-linked fibrin degradation products)]. 177 52

We have studied the potential thrombogenicity of two different heat-treated prothrombin complex concentrates (PCC) in patients with Haemophilia B. Seven patients were studied on nine separate occasions. Four of the patients had chronic hepatitis C (HCV) associated liver disease and three were HIV-antibody positive. The PCCs were Profilnine (Alpha Therapeutics, Thetford, UK) and 9A (Bio-Products Laboratory, Elstree, UK) and the dose administered ranged from 35 to 60 U/kg. Blood samples were taken on ten separate occasions; twice before the infusion and at 15, 40, 60, 75 and 120 min and 4, 8 and 24 h after the infusion of PCC. Investigations included prothrombin time, kaolin cephalin clotting time, thrombin time, fibrin(ogen) degradation products, factor VIII, factor IX, antithrombin III and fibrinopeptide A (FPA). Fibrinopeptide A rises were seen following two of six infusions of 9A and one of three infusions of Profilnine. On all three occasions the rise in FPA was transient, returning to baseline levels within 120 min. Plasma beta-thromboglobulin (BTG) was assayed in three patients and in one patient, the rise in FPA was followed by an increase in BTG. No other changes were observed and there were no clinical features of disseminated intravascular coagulation. Our results indicate that even with normal clinical doses of PCC, intravascular thrombin generation can occur in patients with Haemophilia B. However, this effect is inconsistent both with respect to PCC batch and patient, but may occur in the absence of HIV infection and HCV liver disease.
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PMID:Potential thrombogenicity of heat-treated prothrombin complex concentrates in Haemophilia B. 178 33

The study of immune and fibrinolytic systems in 216 atherosclerosis patients with associated chronic obstructions of the lungs revealed a discrete pattern of activity of plasminogen activator which is low in atherosclerosis in contrast to its elevation in combination of atherosclerosis with pulmonary obstructions. The latter cases manifest E-RFC relative number to be reduced in increased number of EAC-RFC. Growing amount of EA-RFM, elevated blood antithrombin III, activation of plasminogen activator in atherosclerosis coexistence with obstructive pulmonary lesions arrest the development of latent DIC syndrome and progression of atherosclerosis.
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PMID:[Changes in immune and fibrinolytic systems of patients with atherosclerosis and chronic nonspecific pulmonary diseases]. 178 74

Prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complexes (TAT), as well as other coagulation and fibrinolysis parameters, were studied in a series of 13 patients affected by thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS). Fragment F1 + 2 was found to be increased in all patients at diagnosis (patients' range, 1.21-19.03 nmol/l; normal limits, 0.28-1.08 nmol/l), and remained also higher than normal after treatment with plasma exchange (patients' range, 1.5-4.01 nmol/l). Even though the analysis of fibrinolysis markers did not show a definite state of hypo or hyperfibrinolysis in the systemic circulation, enhanced circulating D-dimer levels (0.53-12.6 micrograms/ml, normal levels of 0.03-0.29 micrograms/ml) indicated that a certain grade of fibrin lysis was present at previously formed thrombi. Plasma PAI-1 activities either on admission (9.2-38.2 U/ml) and after plasma exchange therapy (2.6-38.6 U/ml) showed a behavior irrespective of t-PA:Ag changes, and post-plasmapheresis values remained high only in patients with fatal neurological outcome. Nevertheless, no correlations between clinical and laboratory data could be established useful for the TTP/HUS prognosis. We conclude that increased thrombin generation occurring in damaged areas is appropriately inhibited by antithrombin III in the systemic circulation, avoiding consumption coagulopathy to develop in uncomplicated patients. In addition, fibrinolysis data suggest that elevated PAI-1 may decisively favor the development of microvascular thrombi.
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PMID:Thrombin generation and fibrinolysis in the thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. 151 82


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