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

In order to assess the thrombin and plasmin generation in vivo in disseminated intravascular coagulation (DIC), plasma levels of thrombin-antithrombin III (ATIII) complex (TAT) and plasmin-alpha 2-antiplasmin (a2AP) complex (PAP) were measured together with standard coagulation and fibrinolytic parameters in 80 patients with DIC. Both TAT and PAP were markedly elevated in patients with DIC. When plotted by the underlying disease categories, differences in the magnitude of the elevations of these complexes were recognized among groups. Patients with acute promyelocytic leukemia (APL) had the highest PAP, the lowest TAT/PAP ratio, low a2AP, and low fibrinogen, indicating that the most excessive fibrinolysis can occur in APL. Similar profiles, although less marked, were observed in patients with other leukemias and vascular diseases. Patients with sepsis showed the highest TAT/PAP ratio and the lowest PAP with no decrease in a2AP or fibrinogen, demonstrating a relatively impaired fibrinolysis. Patients with cancer had a relatively high TAT and high TAT/PAP ratio. In addition, both TAT and PAP were markedly elevated in patients with shock. From these, it was suggested that, although laboratory manifestations in DIC are extremely variable from patient to patient, underlying disorders are, at least in part, responsible for the observed variations. Recognition of this variable activation of coagulation and fibrinolysis would be helpful for the proper management of patients with DIC.
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PMID:Thrombin vs. plasmin generation in disseminated intravascular coagulation associated with various underlying disorders. 200 32

A new method for estimation of the time course of prothrombinase-thrombin activity is suggested. The method is based on approximation of the autocoagulogram appropriate section to the regression straight line and estimation of the angular coefficient B. This coefficient more accurately reflects the rate of the prothrombinase-thrombin activity growth and decline. The method is time-saving and simple, it is recommended for estimation of functional activity of hemostasis major component and of the principal marker of thrombin formation, the blood disseminated intravascular coagulation.
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PMID:[Mathematical assessment of the blood prothrombinase-thrombin activity by the autocoagulation test]. 169 27

We studied the quantitative changes of hemostatic molecular markers with time during the course of disseminated intravascular coagulation (DIC) induced by endoscopic embolization using thrombin for esophageal varices in nine patients with liver cirrhosis. The plasma levels of D-dimer, a product of plasmin degradation of cross-linked fibrin, and thrombin-antithrombin-III complex (TAT) were significantly higher in patients before treatment when compared with 60 healthy individuals. The plasma levels of TAT, D-dimer, and plasmin alpha 2-plasmin inhibitor complex (PIC) increased significantly 5-15 min after thrombin injection into the varices, earlier than the changes of conventional coagulofibrinolytic factors, reached a maximum level after 180 min, and started to decline after 1 day. Although the plasma PIC level returned to normal after 7 days, both TAT and D-dimer were still above the pretreatment level. Although there was no change in urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA) increased significantly after 5 min. The plasma level of plasminogen activator inhibitor type 1 (PAI-1) showed only a slight elevation after treatment. We propose that the hemostatic molecular markers TAT, D-dimer, and PIC are suitable for the early diagnosis of DIC after endoscopic embolization using thrombin in patients with liver cirrhosis and that the increase of PAI-1 is too small for the regulation of fibrinolysis due to t-PA in DIC occurring in liver cirrhosis.
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PMID:Significance of hemostatic molecular markers during disseminated intravascular coagulation in patients with liver cirrhosis treated by endoscopic embolization for esophageal varices. 171 8

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


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