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)

An assay measuring the thrombin inactivating effect of human plasma in the presence of dermatan sulfate (DS) is described. Test plasma, diluted 1/50, is incubated with human thrombin in the presence of DS. Remaining thrombin is determined with chromogenic substrate 2AcOH . H-D-CHG-Ala-Arg-pNA. Three dilutions of reference plasma suffice and the standard curve is linear. Antithrombin III (AT) exerts a small (3-8%) effect in the assay. When test plasma contains heparin above 0.05 U/ml, this unspecific effect of AT increases, but it may be abolished by antibodies against AT. In a normal material (n = 50), the SD of DS cofactor activity was greater (15%) than that of AT (8.7%). DS cofactor was normal in hereditary AT deficiency and in 15 patients with deep venous thrombosis. In liver cirrhosis and in DIC, both inhibitors were markedly depressed, to similar degrees (r = 0.84).
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PMID:Assay of dermatan sulfate cofactor (heparin cofactor II) activity in human plasma. 654 86

Protein C, a newly identified inhibitor of blood coagulation, was measured immunologically in 58 patients with untreated acute leukemias and compared with that of normal subjects. On the average, slightly lower values were found. However, the 17 patients with overt laboratory pictures of decompensated disseminated intravascular coagulation (DIC), including 11 cases with acute promyelocytic leukemia, had protein C concentrations no lower than those of the remaining 41 patients without DIC. Antithrombin III activity and antigen were normal and, like protein C, not lowered in DIC. The concentrations of both proteins were closely correlated with changes in the indexes for liver synthetic function. A subgroup of 13 patients with hyperleukocytic leukemias had lower protein C and antithrombin III, in line with the more compromised synthetic function of their livers. Our findings indicate that liver impairment rather than DIC is the main cause of the changes in the two naturally occurring inhibitors of blood coagulation.
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PMID:Liver dysfunction rather than intravascular coagulation as the main cause of low protein C and antithrombin III in acute leukemia. 658 88

Among 113 consecutive patients with disseminated intravascular coagulation (DIC), twenty cases who developed this condition under surgical intervention are the subject of this study. At the onset of DIC, fourteen cases were suffered from severe infection. Coagulation study in these patients revealed decreased platelet counts and prolonged prothrombin time. There was marked increase in fibrinogen degradation products and positive ethanol gelation test was frequently observed. These findings were analogous to those found in the more chronic presentations of DIC in the patients with neoplastic diseases, however, plasma concentration of fibrinogen was normal. Antithrombin III level was extremely low in the patients with surgical DIC. The patients with DIC in surgery took acute or subacute courses with very high incidence of major organ failure. The patients with dysfunction of more than three organs were seen in eight of 20 cases. The lungs, kidneys, liver and gastrointestinal tracts were involved in the descending order of frequency. Fourteen patients died and six of these were autopsied. All had multiple fibrin thrombi in more than two organs. The numbers and sites of microthrombi in the major organs were well matched with the clinical manifestations. These results suggested that DIC might be one of the precipitating factors of multiple organ failure.
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PMID:[A clinical study on surgical patients with disseminated intravascular coagulation: with special reference to the occurrence of major organ failures]. 667 56

Antithrombin III (AT-III) is the major inhibitor of thrombin, Factor Xa, and other coagulation enzymes. Congenital and acquired deficiencies of AT-III are thought to contribute to thrombosis and disseminated intravascular coagulation. Because a recent report suggested reduced AT III in stored blood, we evaluated blood bank storage effects. Serial samples were taken from 6 units of whole blood drawn into citrate-phosphate-dextrose-adenine over 42 days, and assays for AT-III functional activity were performed on the same day. The values (mean +/- SD) were as follows: day 0,91.8 +/- 10.7 percent; day 2, 101.9 +/- 10.7 percent; day 8, 107.3 +/- 7.4 percent; day 15, 118.9 +/- 11.1 percent; day 22, 105.4 +/- 9.8 percent; day 35, 93.4 +/- 8.8 percent; and day 42, 97.4 +/- 7.5 percent. The rise from day 0 to day 15 was significant but presumably secondary to interassay variation because analysis of frozen aliquots showed no significant change when all samples from each unit were assayed in one batch. Immunoassay of AT-III also showed no change with storage. The results indicate AT-III retains functional activity in whole blood stored at 2 to 6 degrees C for 42 days, and AT-III replacement does not require fresh blood or fresh-frozen plasma. Low values may reflect individual donor differences or dilution of plasma by anticoagulant.
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PMID:Preservation of antithrombin III activity in stored whole blood. 669 39

Antithrombin III (At III) levels in plasma samples were determined by incubation of diluted plasma with thrombin, either with or without heparin. Followed by measurement of residual thrombin using clotting and amidolytic methods. All assays were of multidose bioassay design suitable for parallel line analysis. Assays without heparin showed only a small difference between amidolytic and clotting methods, which was not significant at the 95% level. Assays with heparin showed a much larger difference between clotting and amidolytic methods which is shown to be attributable to the heat defibrination step used in the clotting assay. Heat defibrination and ancrod defibrination methods are compared using the amidolytic heparin cofactor assay and it is shown that heat defibrination can cause the loss of nearly 50% of the functional At III in a reconstituted freeze-dried plasma which was used as a standard. No loss occurs when ancrod is used for defibrination. It is an advantage of the amidolytic heparin cofactor assay that defibrination is not required.
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PMID:Comparison of antithrombin III assays using biological and chromogenic substrates. 705 31

In 15 patients admitted to the Intensive Care Unit for shock and with signs of DIC, Antithrombin III (AT III) was substituted. Immediately after the first blood sampling, 1,000 units of AT III was given. This was followed by 500 units AT III after 24 h and after 48 h. A continuous dose of heparin of between 250 and 500 I.U./h was simultaneously given. The following results were obtained: The activity of AT III on admission of 63 +/- 19% increased to 83 +/- 17% 30 min after the initial substitution. There was a clear difference between the recovery of the substituted AT III in acute DIC and in patients in a steady state. AT III recovered in circulation was 47 +/- 15% in the former group but 83 +/- 16% in the latter cases. One unit of AT III per kg body weight increased AT III activity in circulation by 1% in acute DIC but by 1.8% in a steady state. The average half life of the substituted AT III was 4.4 +/- 1.6 h in acute DIC and was 20.2 +/- 4.1 h when the patients were in a steady state.
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PMID:Substitution therapy with an antithrombin III concentrate in shock and DIC. 713 59

Antithrombin III (AT III) an alpha 2 globulin produced by liver, is the most important plasmatic inhibitor of activated coagulation factors, that bind irreversibly to it with formation of inactive complexes. Therefore, when coagulation processes are activated in vivo, a decrease of AT III is presumably likely to occur. In the present research, AT III has been determined both as substance concentration, by radial immunodiffusion, and on the base of its activity on a chromogenic substrate (Chromozym) in patients with DIC before and after heparin therapy. Some patients with acute liver insufficiency have been similarly studied, because they not only have a deficient protein synthesis but also show phenomena of anticoagulative factors consumption. In all the patients, the AT III levels appeared decreased by both methods; the decrease of activity was comparatively much more intense and in a case no activity was even detectable.
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PMID:[Clinical importance of the determination of antithrombin III by the use of a chromogenic substrate, in cases of disseminated intravascular coagulation and of acute hepatic insufficiency]. 726 80

Antithrombin III-heparin cofactor has now been recognized as a major inhibitor of thrombin and other serine proteases in the blood coagulation system. Since the reaction between antithrombin III and serine proteases is irreversible, one would expect antithrombin III consumption in the face of pathologic intravascular coagulation and attendant generation of thrombin, IXa, Xa, XIa, XIIa, and plasmin. Using a new assay system for antithrombin III that is unaffected by heparin or fibrino (geno) lytic degradation products, antithrombin III was monitored before and during therapy in 38 patients who had acute or chronic disseminated intravascular coagulation. It was found that early and significant decreases in anththrombin III occur in disseminated intravascular coagulation and thus may serve as a useful diagnostic tool. It was further found that monitoring antithrombin III during therapy reflected a cessation of antithrombin III consumption and, thus, served as an indicator of the efficacy of therapy in stopping the clotting process. Since the assay system is unaffected by fibrino(geno)lytic degradation products and heparin, it proved useful in monitoring the efficacy of heparin therapy for disseminated intravascular coagulation. In addition for this group of patients, it appeared that mini-heparin therapy and large doses of heparin were equally efficacious in correcting other laboratory abnormalities of disseminated intravascular coagulation, and in controlling clinical hemorrhage in disseminated intravascular coagulation.
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PMID:Antithrombin III patterns in disseminated intravascular coagulation. 736 82

Treatment of acute promyelocytic leukemia (APL) patients with all-trans retinoic acid (ATRA) was associated with rapid improvement in hemostatic markers. We made serial analyses of various hemostatic parameters in seven newly diagnosed APL patients. In all patients at diagnosis, plasma fibrinogen/fibrin degradation product (fragment-E), cross-linked fibrin degradation product (D-dimer fragment), thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex were elevated, indicating the presence of disseminated intravascular coagulation (DIC). Antithrombin III (ATIII) levels were normal in all patients except for the patient with congenital ATIII deficiency. In four patients subsequently treated with ATRA without anticoagulant therapy, these hemostatic markers returned to near-normal levels by day 7 of treatment, indicating that DIC was essentially resolved. By contrast, in three patients who received conventional chemotherapy with a continuous low-dose heparin, improvement of coagulopathy was slower than in patients treated with ATRA. These results suggest that ATRA therapy exerts the rapid improvement in abnormal hemostatic markers in APL patients without any anticoagulant therapies, by inducing differentiation of leukemic cells and, in turns no massive release of procoagulant or fibrinolytic substances from these cells.
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PMID:Rapid improvement of coagulopathy by all-trans retinoic acid in acute promyelocytic leukemia. 819 47

In the development of sepsis DIC is a common complication. Several studies presented in this paper show a coincidence between the development of DIC and depletion of Antithrombin III, a serine protease inhibitor which inhibits a large scale of activated clotting factors. It seems very probable that substitution therapy should be of benefit in the treatment of sepsis-related DIC and may improve the outcome of septic patients. Physiological and clinical findings are put together to clarify the basic rationale for running clinical trials and future studies.
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PMID:AT III in septicemia with DIC. 822 35


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