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)

Recently, monoclonal antibody (DD-3B6) to fibrin D-dimer was prepared and coupled to latex beads to provide a specific test (Dimertest) for fibrinolysis. The purpose of this study was to evaluate the Dimertest assay as a clinical laboratory test for the measurement of plasma fibrin D-dimer derivatives. The Dimer-test assay specifically detected 2 micrograms/mL of purified fibrin D-dimer or fibrin D-dimer/fragment E complex added to afibrinogenemic plasma but did not detect 500 micrograms/mL of either fibrinogen fragments X, D, E, or 160 micrograms/mL cross-linked fibrinogen. The fibrin(ogen) degradation product (FDP) assays of American Dade or Wellcome Diagnostics detected 5.0 micrograms/mL of fibrin D-dimer and from 1 to 10 micrograms/mL of the other FDPs. Twenty-eight percent of 150 random plasma samples assayed from hospitalized patients were positive for fibrin D-dimer derivatives. Plasma samples from 152 patients suspected of having disseminated intravascular coagulation (DIC) were assayed for serum FDP (Wellcome Diagnostics) and plasma fibrin D-dimer derivatives. Samples from 69% of patients with serum FDP levels less than 10 micrograms/mL, and more than 90% of those with serum FDP levels greater than 10 micrograms/mL, were positive for fibrin D-dimer derivatives. Dimertest results were not modified by heparin, streptokinase, freeze-thawing, or clotting plasma. Serum fibrinogen-related antigens were immunoadsorbed from Dimer-test positive sera by anti-fibrinogen antibody and formalin-fixed Cowan I strain Staphylococcus aureus. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and protein blotting with the use of monoclonal antibody DD-3B6 demonstrated a protein band with similar mobility to purified D-dimer. The measurement of plasma fibrin D-dimer derivatives by the Dimertest assay is a rapid, sensitive, and specific laboratory test for fibrinolysis. The Dimertest assay has proven to be a useful addition to the clinical laboratory and should be helpful in the diagnosis and management of patients with diseases associated with fibrinolysis.
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PMID:Measurement of plasma fibrin D-dimer levels with the use of a monoclonal antibody coupled to latex beads. 354 76

In vitro coagulation produces a consumption of heparin co factor II (HC II) of 8-10% both in plasma from normal individuals and patients whereas antithrombin (AT) consumption ranges 40-50%. In blood from heparin treated patients consumption is similar or greater. In blood from warfarin treated patients, consumption is decreased. Addition of heparin prior to clotting has little effect on HC II consumption, but high heparin concentration reduces AT consumption. Addition of dermatan sulfate has no effect on AT consumption, but increases HC II consumption dramatically. In consumption coagulopathy, the HC II levels are as low as AT, possibly reflecting intravascular consumption accelerated by vascular glycosaminoglycans.
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PMID:Consumption of heparin cofactor II (dermatan sulfate cofactor) and antithrombin during coagulation. 360 28

The apoprotein (AP) of tissue factor (TF) has been purified 72,000-fold to homogeneity from human placenta using acetone delipidation, sodium deoxycholate (DOC) extraction, Sephacryl S-300 column chromatography, preparative polyacrylamide-gel electrophoresis (PAGE) in DOC and tryptic digestion. The purified AP had an apparent molecular weight of 54,000 by sodium dodecyl sulfate/PAGE. A radioimmunoassay (RIA) for quantitation of the TF-AP using an antibody against this purified AP of TF was devised which was sensitive enough to measure as small a quantity as 100 pg/ml of TF-AP accurately with high reproducibility. In addition to TF clotting activity (TFA), the immunoreactive TF-AP (IR-TFR) in the homogenates of leukemic leukocytes from patients with acute non-lymphoid leukemia (ANLL) was determined using this RIA. In 30 patients with ANLL, the mean IR-TFR with standard deviation (SD) of 21 cases with DIC was 157.9 +/- 188.1 ng/10(8) cells, which was significantly higher than that (37.1 +/- 29.9 ng/10(8) cells) of 9 cases with no DIC during remission induction chemotherapy (p less than 0.01).
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PMID:Radioimmunoassay of human tissue factor. 373 65

An electrophoretic method has been applied to characterize specific fibrinogen and fibrin degradation products (FDP) in 135 serum samples from 59 consecutive patients having a positive latex agglutination test for serum FDP in the evaluation of consumption coagulopathy. In 20 of 135 positive samples, the principal fibrinogen derivatives present were not degradation products of fibrinogen or fibrin but were instead residual fibrinogen or fibrin monomer and polymers (FFMP) due to incomplete clotting. Heparin exposure was common in patients with positive FDP tests occurring in 29 of 59 patients (49%) with 81 of 135 samples (60%). Heparin exposure by parenteral administration or catheter was significantly correlated with a false positive serum FDP test because of residual FFMP occurring in 19 of 81 (23%) samples from heparin-exposed patients but in only 1 of 54 (2%) samples from patients without exposure (P less than 0.005). Treatment of the false positive samples with reptilase, an enzyme unaffected by heparin, resulted in complete removal of the residual FFMP, and in vitro experiments demonstrated that heparin-containing plasma samples could be completely clotted with either reptilase or protamine sulfate plus thrombin. Survey of 20 regional laboratories showed that only 10% used reptilase or protamine sulfate to prepare serum if heparin exposure had occurred and that this was done in only 22 of 5,049 (0.4%) of samples in the last calendar year. Greater attention should be given to proper preparation of serum from heparin-exposed patients, and physicians should be aware of the possibility of falsely positive or falsely elevated serum FDP tests in evaluation of consumption coagulopathy in heparin-exposed patients.
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PMID:Prevalence and clinical implications of heparin-associated false positive tests for serum fibrin(ogen) degradation products. 375 95

The informative value of each of 15 laboratory indices (the amount of platelets, their factor 4 (PF-4), antithrombin III (AT III), fibrinogen and its degradation products (FDP), ethanol and protamine sulfate tests (ET, PST), plasminogen, the eucaryne test, etc.), most commonly used now in laboratory practice for the diagnosis of the DIC syndrome was assessed using mathematical methods relating mainly to the theory of pattern recognition. Basic and alternative algorithms of the recognition of the DIC syndrome which could be used with a minor error (less than or equal to 2.5% and less than or equal to 7-10% respectively) irrespective of the type, form and stage of this syndrome both in the automated system and in a common variant, were developed. Their testing was successfully implemented in a large group of patients with symptoms of the DIC syndrome (770 persons). Indices of the platelet amount, FDP, PF-4,ET and PST possessed the utmost informative value, and close functional ties were particularly noticeable between elevated FDP and lowered platelets. Optimum combinations of the diagnostic indices were presented and substantiated with relation to the potentialities of different types of laboratories.
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PMID:[Diagnostic criteria in the DIC syndrome and their validation using modern mathematical methods]. 378 83

Intravenous injection of homologous lung or brain tissue thromboplastin in dogs under general anesthesia induced changes of conventional hemostasis variables consistent with acute DIC (prolongation of prothrombin times, thrombin times, APTT, drop of fibrinogen and a transient reduction of the platelet count). The animals reacted with accelerated respiration and pulse rates. After recovery from anesthesia they resumed their normal activity as before. Fibrinogen reached a minimum within 40 min after the DIC trigger dose had been injected. Dependent on the size of the latter up to 80% of clottable fibrinogen was consumed. No consumption of antithrombin III and heparin cofactor II could be demonstrated by functional assays based on thrombin inhibition by diluted plasma in the presence of heparin or dermatan sulfate. Prothrombin measured amidolytically by an Echis Carinatus venom assay remained practically unchanged. These findings are consistent with free thrombin concentrations in the nanomolar range sufficient to clot fibrinogen rapidly without visibly affecting the up to 1,000 fold higher concentrations of inhibitors and prothrombin. Heparin administered before tissue thromboplastin virtually suppressed the evolution of DIC but its protective effect was overcome by higher trigger doses. Heparin injected after the induction of DIC had no protective effect. The reversible DIC model in dogs may be a promising tool to study activated coagulation in vivo at practically constant inhibitor concentrations. One dog can be used for several acute experiments with homologous tissue thromboplastin, thus the number of animals and their costs may remain within reasonable limits.
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PMID:Heparin-enhanced inhibitors during reversible disseminated intravascular coagulation. 386 25

A novel platelet-agglutinating protein (PAP) was purified approximately 2,000-fold from the plasma of a patient with thrombotic thrombocytopenic purpura (TTP) by ammonium sulfate fractionation, DEAE-Sephacel and concanavalin A-Sepharose chromatographies. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, with and without reduction, this preparation revealed a major protein band with a molecular weight of 37,000, and a minor band with a molecular weight of 32,000-34,000. After elution from the gel, only the 37,000-mol wt protein corresponding to the major band induced the platelet agglutination. When four normal plasmas and the recovery plasma from the same TTP patient were subjected to the similar purification steps, the 37,000-mol wt major band was absent. The 125I-PAP bound to the platelets in a concentration-dependent manner. The platelet agglutination induced by PAP was not inhibited by hirudin, heparin in the presence of antithrombin III, phenylmethylsulfonyl fluoride, apyrase, aspirin, or prostaglandin I2. However, it was inhibited by IgG from normal adults and from the same TTP patient after recovery. The anti-37,000-mol wt PAP antiserum prepared in the rabbit formed a single precipitin line against the highly purified PAP. Using this antiserum in the Western immunoblotting, the 37,000-mol wt protein band was found in the three TTP plasmas, of which the platelet-agglutinating activity was inhibited by the anti-37,000-mol wt PAP IgG. The 37,000-mol wt immunoprecipitin band was absent in the plasmas obtained from another two TTP patients, two normal subjects, two patients with idiopathic thrombocytopenic purpura, and two patients with disseminated intravascular coagulation. These results suggest that the 37,000-mol wt PAP is present only in certain cases of TTP, and is likely to be responsible for the formation of platelet thrombi in the microcirculation.
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PMID:Novel platelet-agglutinating protein from a thrombotic thrombocytopenic purpura plasma. 393 64

Factor VIII antigen (VIII:CAg) exhibits molecular weight heterogeneity in normal plasma. We have compared the relative quantities of VIII:CAg forms present in normal individuals (n = 22) with VIII:CAg forms in renal dysfunction patients (n = 19) and in patients with disseminated intravascular coagulation (DIC; n = 7). In normal plasma, the predominant VIII: CAg form, detectable by sodium dodecyl sulfate polyacrylamide gel electrophoresis, was of molecular weight 2.4 X 10(5), with minor forms ranging from 8 X 10(4) to 2.6 X 10(5) D. A high proportion of VIII:CAg in renal dysfunction patients, in contrast, was of 1 X 10(5) mol wt. The patients' high 1 X 10(5) mol wt VIII: CAg level correlated with increased concentrations of serum creatinine, F1+2 (a polypeptide released upon prothrombin activation), and with von Willebrand factor. Despite the high proportion of the 1 X 10(5) mol wt VIII:CAg form, which suggests VIII:CAg proteolysis, the ratio of Factor VIII coagulant activity to total VIII:CAg concentration was normal in renal dysfunction patients. These results could be simulated in vitro by thrombin treatment of normal plasma, which yielded similar VIII:CAg gel patterns and Factor VIII coagulant activity to antigen ratios. DIC patients with high F1+2 levels but no evidence of renal dysfunction had an VIII:CAg gel pattern distinct from renal dysfunction patients. DIC patients had elevated concentrations of both the 1 X 10(5) and 8 X 10(4) mol wt VIII:CAg forms. We conclude that an increase in a particular VIII:CAg form correlates with the severity of renal dysfunction. The antigen abnormality may be the result of VIII:CAg proteolysis by a thrombinlike enzyme and/or prolonged retention of proteolyzed VIII:CAg fragments.
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PMID:Abnormal factor VIII coagulant antigen in patients with renal dysfunction and in those with disseminated intravascular coagulation. 393 66

A new method is described for identifying low concentrations of circulating derivatives of fibrinogen and fibrin, even when present in heterogeneous mixtures. This technique is applicable to plasma and serum and uses electrophoresis in 2% agarose in the presence of sodium dodecyl sulfate (SDS) followed by immunological identification of separated derivatives, using radiolabeled antifibrinogen antiserum and autoradiography. Unique electrophoretic patterns distinguish plasmic derivatives of crosslinked fibrin from those of fibrinogen and also identify crosslinked fibrin polymers produced by the combined action of thrombin and factor XIII on fibrinogen. The assay is sensitive to a concentration of 0.1 micrograms/mL of fibrinogen in serum or plasma. Fibrin polymers, plasmic degradation products of fibrinogen, and plasmic degradation products of crosslinked fibrin were detected in the plasma or serum of a patient with disseminated intravascular coagulation. Plasmic derivatives of both fibrinogen and crosslinked fibrin appeared in serum in the course of fibrinolytic therapy for pulmonary embolism, whereas during acute myocardial infarction a marked increase in the proportion of fibrin polymers in plasma was found in comparison with normal controls. Thus, the procedure can distinguish between the simultaneous processes of fibrin polymer formation, fibrinogenolysis, and fibrinolysis, and is sufficiently sensitive to detect relevant quantities of derivatives in pathologic conditions.
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PMID:Specific identification of fibrin polymers, fibrinogen degradation products, and crosslinked fibrin degradation products in plasma and serum with a new sensitive technique. 397 Oct 42

The coagulation and fibrinolytic function of 100 cases (male 75, female 25) of trauma limited to the head was evaluated in acute phase. The coagulation and fibrinolytic function was evaluated by 6 parameters, consisting of platelet counts, PT, APTT, fibrinogen, serum FDP, and protamine sulfate test. Head injury was categorized into 5 groups according to CT findings: subdural hematoma (SDH: 13 cases), cerebral contusion (CC: 46 cases), epidural hematoma (EDH: 21 cases), skull fracture only (Fr: 14 cases), and cerebral concussion (Co: 6 cases). The results were as follows, in 19 dead cases, severe coagulopathy was observed. In intracerebral injury group (SDH + CC), serum FDP level was markedly elevated. The incidence of disseminated intravascular coagulation (DIC) following head injury was 24% (in dead cases 73.7% in survival cases 12.3%) of all cases, and mortality of cases with DIC was exceedingly high (58.3%). In 14 dead cases with DIC, the patients did not recover from DIC, and their mean survival time was only 89.2 hours. In 10 survival cases with DIC, the patients recovered from DIC. APTT was the most important to estimate the mortality of head injury. Thus, the evaluation of coagulation and fibrinolytic function in head injury in acute phase is not only important to know the occurrence of DIC, but also useful to predict the severity and prognosis of head injury.
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PMID:[Disturbance of the coagulatory system in patients with head injury in acute phase]. 398 95


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