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)

The article reports on measurements of D dimer, a terminal plasmic lysis product of crosslinked fibrin, with an enzyme immunoassay (ELISA) employing recently developed specific monoclonal antibodies. Due to its sensitivity the test can be used on plasma samples. The D dimer concentrations in patients with deep vein thrombosis diagnosed by laboratory apparatus were significantly increased compared to a control group; in one patient with additional pulmonary embolism, the level was even higher. Moderately elevated concentrations of D dimer were observed in the hypercoagulable state of pregnancy, puerperium and during the postoperative course. This reduces the specificity of the test with regard to the recognition of thromboembolic episodes under these conditions. Obstetric patients with disseminated intravascular coagulation (DIC) showed excessively increased levels of D dimer. Hence, a marker function with regard to the recognition of thromboembolic disease can be attributed to the D dimer; the diagnosis of DIC can be confirmed if very high concentrations are detected.
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PMID:[A test for the detection of fibrin in the plasma]. 395 64

125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
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PMID:Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency. 400 29

The effect of a low-dosage regimen of ancrod in the prevention of postoperative deep vein thrombosis was assessed in 24 patients having surgical repair of fractured neck femur and compared with 25 control patients who did not receive therapy. The objective of the therapy was to lower the preoperative fibrinogen level and produce a low concentration of fibrin degradation products yet avoid the haemorrhagic complications of total defibrination. Ancrod therapy proved feasible to carry out, was not associated with haemorrhagic complications, and produced sustained, predictable reductions in fibrinogen concentration. There were seven thromboembolic complications in the control patients compared to one such complication in the ancrod-treated patients. Five deaths occurred in the control group and one in the treated group. Though the incidence of deep vein thrombosis was not apparently affected by ancrod it appeared on venography that the thrombi in the treated patients were less extensive than those in the control patients. Finally, some discrepancies in the diagnosis of deep vein thrombosis by the three techniques of clinical examination, (125)I-fibrinogen scanning, and ascending venography were identified.
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PMID:Low-dosage ancrod for prevention of thrombotic complications after surgery for fractured neck of femur. 460 45

In patients with acute deep vein thrombosis of the pelvis and limbs and in patients with decompensating course of DICFS considerable defects in AT III function are regularly demonstrated by laboratory tests, while in groups including patients with old or less pronounced venous thrombosis or in patients with compensated or overcompensated consumption coagulopathy normal AT III values might frequently be expected. This seems to be of interest for the interpretation of laboratory data on AT III. However, from these findings AT III replacement cannot be deduced and they cannot be used as a criterion to assess the prognostic value of AT III deficiency for the course of the underlying disease. In acquired AT III defects the anticoagulant activity of heparin is not necessarily decreased. After continuous infusion of doses below 500 USP in patients with DICFS and after administration of heparin doses of 750 USP/h/70 kg in patients undergoing fibrinolytic therapy the AT III content rather increases continuously. After extremely high heparin doses during extracorporeal circulation in the heart-lung machine transitorily decreased AT III values return to normal. In certain risk situations, however, such as after bolus injection of comparatively high heparin doses in patients with greatly reduced AT III values, a lowered anticoagulant effect of high heparin doses must be expected. In these cases AT III replacement is indicated. However, when enhanced heparin resistance is suspected or diagnosed, treatment with AT III concentrates is justified only when the diagnosis is based on laboratory findings. Cortisone and protamine chloride were found to exert direct effects on AT III function and concentration independent of the AT III defects mentioned.
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PMID:[Significance of disordered antithrombin III function in disseminated intravascular coagulation and deep venous thrombosis for anticoagulant therapy]. 608 7

Fibrinogen degradation, fibrin polymerisation, and the insertion of cross links into fibrin by fibrin stabilising factor lead to the appearance of new antigenic determinants. Antibodies against these antigenic sites may react specifically with the derivatives but not with the parent molecules. We have utilised a monoclonal antibody, which interacts with the cross linked fragment D dimer and related high molecular weight fibrin derivatives, to develop an enzyme immunoassay which measures cross linked fibrin derivatives in plasma and serum using D dimer as standard. Mean concentration in plasma from normal subjects was 75 ng/ml with an upper limit of about 144 ng/ml. Concentrations in patients with pulmonary embolism, deep venous thrombosis, arterial thromboembolism, and disseminated intravascular coagulation were raised in all cases. Confirmation of the specific increase of cross linked fibrin derivatives in patients with disseminated intravascular coagulation was obtained by parallel monitoring of their fibrin degradation products in serum using affinity chromatography and sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. In many patients the plasma concentrations greatly exceeded the serum values of cross linked fibrin degradation products, suggesting that the procedure can measure fibrin derivatives in plasma which are absent from serum.
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PMID:Measurement of cross linked fibrin derivatives in plasma: an immunoassay using monoclonal antibodies. 620 97

The purpose of these studies was to establish the validity of 125I fibrin autoradiography--SDS gel techniques for monitoring degradation products from whole plasma or blood clots. These methods can be used to study fibrin degradation not only in patients with congenital factor XIII deficiency, but also in patients with disseminated intravascular coagulation or deep vein thrombosis during the course of thrombolytic therapy. Such an assay might complement existing immunologic techniques to characterize fibrin degradation in vivo by providing an in vitro analysis of the rate and pattern of fibrin degradation in whole blood or plasma. Fibrin degradation was traced by Coomassie blue staining for protein and by autoradiography on SDS-PAGE of degradation products released from a 125I-labeled fibrin tracer. The degradation of non-crosslinked clots from purified fibrin supplemented with plasmin showed a typical release of X, Y, D, and E fibrin fragments. Subsequently, all X and Y fragments were digested to D and E fragments. The degradation of non-crosslinked washed clots prepared from plasma supplemented with plasmin reflected the same pattern. The degradation of non-crosslinked washed clots prepared from EDTA anticoagulated plasma without added plasmin also showed release of X, Y, D, and E fragments. However, in contrast to the non-crosslinked washed clots supplemented with plasmin, there was no additional degradation of the X and Y fragments. These studies established that the pattern of degradation of the 125I-radiolabeled fibrin tracer was similar to that of the total protein released from the fibrin clot as observed by protein staining.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of crosslinking on the structure of solubilized fibrin degradation products in whole plasma. 623 29

We have prepared a monoclonal antibody which recognises an antigenic determinant on D dimer, a specific fragment resulting from the degradation of crosslinked fibrin. This antibody has been used in the development of an enzyme-linked immunoassay for D dimer and related degradation products containing crosslinked gamma-gamma chains, to provide a simple assay of circulating crosslinked fibrin degradation products suitable for clinical use. Since these crosslinked fibrin degradation products are characteristic of fibrinolysis, as distinct from fibrinogenolysis, their measurement should aid in the diagnosis, evaluation and monitoring of thrombotic and thrombolytic states. In preliminary studies, low concentrations of crosslinked fibrin derivatives were detected in normal sera. High levels were found in 30/30 patients with disseminated intravascular coagulation and in the majority of patients having deep venous thrombosis or pulmonary embolism.
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PMID:Measurement of crosslinked fibrin degradation products - an immunoassay using monoclonal antibodies. 635 56

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

Measurement of fibrinogen-fibrin degradation products (FDP) levels in plasma may provide a direct index of plasmin action, and increased levels of FDP would indicate coagulopathy. We have established an E-neoantigen radioimmunoassay ( Eneo RIA) that can determine normal and pathological plasma levels of E-related FDP. The assay employs rabbit antiserum produced against fragment E derived from a plasmin digest of fibrinogen and subsequently absorbed with fibrinogen. The absorbed antiserum contains antibodies which are equally reactive with fibrinogen derived E (Fg-E) and fibrin derived E (Fb-E) but not with fibrinogen at 1 mg/ml. The Eneo RIA was validated by assay parallelism and by recovery experiments. Plasma Eneo immunoreactivities in 14 normals were 4-22 ng/ml (mean 12.7 ng/ml). Plasma Eneo levels in 23 of 24 patients with neoplastic and haematological diseases were elevated above normal (range 27-2027 ng/ml). Unusually high Eneo values were observed with three patients whose diseases were complicated by either disseminated intravascular coagulation (DIC) or deep vein thrombosis. After heparin therapy, the Eneo level of a patient with chronic DIC declined. A pathological plasma was eluted from a Sephadex G-200 column and Eneo immunoreactivity was determined on the eluates. The gel filtration pattern of Eneo indicates that E-related FDP is a family of plasmic fragments derived from crosslinked fibrin.
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PMID:Radioimmunoassay of fragment E-related neoantigen: validation studies and clinical application. 672 32

A fatal case of Streptococcus equisimilis pneumonia and septicemia is described in a young man with Hodgkin's disease. The disease course consisted of exudative pharyngitis, macular rash, septic shock, disseminated intravascular coagulation, deep vein thrombosis, and pulmonary embolization. S. equisimilis was isolated from blood, throat, and sputum cultures antemortem and from lung cultures at autopsy.
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PMID:Streptococcus equisimilis Pneumonia in a compromised host. 683 89


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