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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 summary, this series of 48 patients with acute and chronic DIC demonstrates the reliability of laboratory tests in both aiding a diagnosis of DIC and in offering reasonable predictability of efficacy of therapy, as noted by the correction of abnormalities after delivery of antiprocoagulant therapy for this syndrome. It appears that the diagnostic tests most likely to aid in diagnosis and to reliably inform the clinician when the intravascular clotting process has been stopped are those that determine the antithrombin-III level, the presence of soluble fibrin monomer, and the finding of elevated fibrin(ogen) degradation products, thrombocytopenia and a prolonged thrombin time in the face of the appropriate type of bleeding in the appropriate clinical setting. In addition, it would appear that mini-dose heparin therapy is highly effective in controlling the intravascular clotting process in acute DIC, whereas antiplatelet therapy utilizing two agents is effective in chronic DIC. In addition, in this population, patients with acute disease demonstrated a 74 percent survival rate and those with chronic disease had a 100 percent survival rate from the disseminated intravascular clotting process.
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PMID:Disseminated intravascular coagulation: a clinical/laboratory study of 48 patients. 694 79

We have evaluated the efficacy of utilizing radioimmunoassays (RIAs) for prothrombin activation fragments (F2/F1 + 2) and for thrombin--antithrombin complex (TAT) in purified systems and in whole blood. During venipuncture, appropriate anticoagulants were employed in order to prevent the generation of thrombin and factor Xa. The RIAs were shown to be specific for F2/F1 + 2 as well as TAT and did not interact with other plasma components. Initially, thrombin generation was studied in a purified human system of prothrombin, antithrombin, factor Xa, and factor V as well as phospholipid and Ca++. Under these conditions, the kinetics of F2/F1 + 2 and TAT generation were virtually superimposable. However, when factor V was omitted from the reaction mixture, a significantly greater amount of F2/F1 + 2 as compared to TAT was observable. Subsequently, prothrombin activation was monitored during the spontaneous coagulation of freshly drawn blood. Throughout the entire course of thrombin generation, the observable rate of formation of F2/F1 + 2 was considerably greater than that of TAT. We have examined the levels of F2/F1 + 2 and TAT in normal individuals. Our studies indicate that the concentrations of F1 + 2 and TAT average 1.97 nM and 2.32 nM, respectively. We have also quantitated the concentrations of F2/F1 + 2 and TAT in patients with disseminated intravascular coagulation. In these individuals, the levels of both components are elevated. However, the ratio of F1 + 2 to TAT ranges from 2.37 to 5.55. Thus, we conclude that under in vivo conditions, prothrombin activation is characterized by the accumulation of a stable precursor, such as prethrombin-2, and that this phenomenon may be related to an alteration of factor V function.
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PMID:Studies of the prothrombin activation pathway utilizing radioimmunoassays for the F2/F1 + 2 fragment and thrombin--antithrombin complex. 707 14

A case study report is presented of a 20 year old black woman with a past history of oral contraceptive (OC) use who developed Budd-Chiari syndrome (hepatic vein thrombosis) associated with decreased levels of antithrombin 3. This combination has not been previously reported. The woman presented on December 28, 1979 with midepigastric pain. She had no previous illnesses, but OCs had been used up to 2 years prior to admission. Shortly after admission the patient became hypotensive, developed oliguric renal failure, and began to rapidly accumulate ascites. During this admission, the patient's transaminase levels abruptly declined. A percutaneous liver biopsy obtained on January 9, 1980 showed centrilobular hemorrhagic necrosis of a severe degree. An inferior vena cavagram was repeated on January 14, 1980 demonstrating hepatic vein thrombosis. Streptokinase, followed by heparinization, was given in an effort to lyse the thrombi, but repeat inferior cavagram on January 24th proved this to be unsuccessful. Thrombosis of the left iliac and left femoral vein then appeared. Because of her apparent "hypercoagulable state," the antithrombin 3 level was measured on January 31st and found to be 27%. A simultaneous serum fibrinogen was 255 mg/dl. Family members (father, mother, and 4 children) were studied. All had normal antithrombin 3 levels, thus excluding a familial defect. The patient gradually improved and was discharged on February 25, 1980 on Coumadin, diuretics, and a 3 g sodium diet. Because of ascites and peripheral edema, a LeVeen shunt was placed on March 25, 1980. At surgery, she was noted to have obstruction of the right internal jugular and right cephalic veins. Because of possible thrombosis in the superior inferior vena cava branches, venography was performed on March 31st and demonstrated thrombosis of the right subclavian, inferior vena cava, and internal iliac veins. Despite the therapy, patient again began to reaccumulate ascites and was readmitted on May 17th. The then nonfunctioning shunt was repositioned in the patient's right atrium. Postoperatively, the patient's course was complicated by DIC. Because heparin induced thromboycytopenia was suspected, heparin was discontinued and Coumadin begun. On June 6th the patient became suddenly short of breath. A lung scan was consistent with pulmonary embolism. She could not be adequately ventilated and died on June 8th. Although the patient discontinued OC use 2 years prior to initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than 6 months' duration, thus raising the possibility of a cause-effect relationship between the OC and thrombotic process. Prospective studies are needed to substantiate the view of a relationship between OC use, antithrombin 3 deficiency, and the Budd-Chiari syndrome.
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PMID:Budd-Chiari Syndrome and antithrombin III deficiency. 710 23

A case of excessive heparin requirement during cardiopulmonary bypass is reported. A patient with sepsis secondary to a myocardial abscess require 13.5 mg x kg-1 of heparin to increase his activated coagulation time to a therapeutic level. This phenomenon might be due to individual variability, lupus vasculitis, septicaemia, repeated thromboembolic phenomenon with hypercoagulable state, or chronic disseminated intravascular coagulation with partial antithrombin deficiency.
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PMID:Excessive requirement for heparin during cardiac surgery. 723 24

During the course of severe coagulopathy in an infant suffering from septicaemia and shock, antithrombin III levels were determined repeatedly before and during substitution therapy with human antithrombin. By mathematical analysis of these data, using a biexponential function, the plasma elimination half-life of the antithrombin III was estimated to be 7.5-10.5 h. Compared with known plasma half-lives of radioactively labelled antithrombin III in adults the increase was five-to ten-fold. This indicates that the significantly decreased levels of antithrombin III in this case of coagulopathy were at least partly due to an accelerated consumption of antithrombin III. The estimation of the plasma elimination half-life of antithrombin III helps to differentiate decreased production from increased consumption in cases of severe coagulopathy. Thus, a more precise diagnosis of disseminated intravascular coagulation can be made whilst taking advantage of substitution therapy and avoiding the hazards of radioactive tracer proteins.
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PMID:Decreased production or increased turnover of antithrombin III in severe acquired coagulopathy? 732 83

Polyethylene glycol(PEG) was used to precipitate fibrinogen to prepare defibrinated plasma in the two stage clotting assay of antithrombin activity. Five percent PEG-8000 precipitated fibrinogen from plasma without loss of antithrombin activity in the defibrinated plasma. Fibrin degradation products(FDP) as high as 640 ug/ml did not interfere the two stage clotting assay using PEG defibrinated plasma possibly because part of FDP was precipitated by PEG in the process of plasma defibrination. The two stage clotting assay was very sensitive to the changes of antithrombin activity in the range of 60%-100% of normal level. The assay was reproducible and correlated with chromogenic assay. The decrease of plasma antithrombin activity in a baboon septic shock model was demonstrated with this assay.
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PMID:Functional assay of plasma antithrombin using polyethylene glycol (PEG) defibrinated plasma. 748 43

Thrombin and plasmin generation were assessed in patients with endemic hepatosplenic schistomiasis (15 hepatosplenomegalic, 15 splenomegalic, 15 with advanced hepatic fibrosis and ascites and 15 hepatosplenic patients with hematemesis). Prolongation of prothrombin time, partial thromboplastin time and thrombin time, thrombocytopenia, hypofibrinogenemia, a decrease in antithrombin III and protein C and S levels and elevation in fibrinopeptide A, D-dimer and thrombin-antithrombin complex levels were detected in all groups. The deficit in hemostatic parameters was more pronounced with the advancement of the disease and was maximal in the hematemesis group. Our data demonstrate an increase in both thrombin and plasmin generation and indicate that low grade disseminated intravascular coagulation may occur in association with endemic Egyptian hepatosplenic schistosomiasis even in the steady state without overt bleeding.
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PMID:Disseminated intravascular coagulation in endemic hepatosplenic schistosomiasis. 748 60

Thrombotic events have been reported in acute lymphoblastic leukaemia patients, especially during or after L-asparaginase administration. A so-called L-asparaginase associated coagulopathy has been well recognized, being characterized by a hypercoagulable state (decrease of antithrombin III, plasminogen, protein C, protein S and increase of prothrombin fragment F1 + 2, thrombin-antithrombin complexes and fibrinopeptide A). The aim of this study was to determine whether the supplementation of antithrombin III (AT-III) concentrates could improve the L-asparaginase associated coagulopathy, thereby blocking the activation of the haemostatic system. In 25 adult patients with acute lymphoblastic leukaemia (M 19, F6, mean age 34 years) antithrombin III (AT-III) concentrates were administered at daily doses of 50 U/kg for 10 consecutive days from the beginning of L-asparaginase therapy (6,000 U/m2/day s.c. for 7 days), given according to the GIMEMA ALL 0288 trial. A marked increase of antithrombin III was recorded on days IV-VIII-XI (P < 0.001). No changes in protein C, protein S, plasminogen, alpha 2-antiplasmin, factor VII and platelet count were observed and there was no increase in markers of hypercoagulability. There was no evidence of disseminated intravascular coagulation. In conclusion, AT-III concentrate supplementation during L-asparaginase therapy, by the achievement of high levels of antithrombin III, is associated with a lack of activation of the haemostatic system and appears to overcome the complex coagulopathy associated with L-asparaginase.
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PMID:Antithrombin III infusion suppresses the hypercoagulable state in adult acute lymphoblastic leukaemia patients treated with a low dose of Escherichia coli L-asparaginase. A GIMEMA study. 751 43

The blood coagulation and fibrinolysis of 33 patients with compensated liver cirrhosis and 31 patients with hepatocellular carcinoma were examined using several markers, namely thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC), antithrombin-III (AT-III) and prothrombin time, and the relationship between these markers, endotoxemia, and TNF-alpha was examined. These patients had no complications due to hepatic failure, such as infections, encephalopathy, ascites, G-I bleeding and clinical DIC. PIC was not elevated, but TAT tended to be elevated in LC and significantly elevated in HCC. AT-III was decreased in LC and HCC, and the blood endotoxin was partly positive in LC and HCC, but was not correlated with AT-III or PT. The TAT level in the blood-endotoxin-positive patients measured by endospecy methods was higher than that in the negative patients, and was significantly correlated with the blood endotoxin level in the LC and HCC patients (r = 0.57, r = 0.88, p < 0.01). No relationship was observed between TNF-alpha and blood endotoxin. In conclusion, (1) blood coagulability was activated already in compensated LC and HCC, but was not connected with fibrinolysis, (2) the activation of coagulability was closely related with endotoxemia, and (3) TNF-alpha was not correlated with blood endotoxin or TAT.
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PMID:[Blood coagulation and fibrinolysis in relation to endotoxemia in liver cirrhosis and hepatocellular carcinoma]. 756 21

Tissue factor pathway inhibitor (TFPI) controls activation of blood coagulation while antithrombin (AT) regulates the final stage. Both inhibitors inhibit the intermediate stage of activation. Subnormal levels of TFPI increase the risk of disseminated intravascular coagulation (DIC) in septic conditions, and the risk of occlusive thrombi over damaged vascular intima or fissured arteriosclerotic plaques. The risk of venous thrombosis is increased by subnormal AT or subnormal activity of the protein C system. In contrast, TFPI may be little involved in the control of deep venous thrombosis. Heparin strongly accelerates AT and releases TFPI to the blood. Both these effects may contribute to the antithrombotic effect of heparin. In septic DIC, heparin may contribute little to quench activation of coagulation. Once hereditary deficiency of TFPI is described, its biological role will be better understood.
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PMID:Relative roles of tissue factor pathway inhibitor and antithrombin in the control of thrombogenesis. 764 20


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