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)

Increased serum fibrinogen degradation product (FDP) in liver cirrhosis and hepatic carcinoma as measured by latex agglutination was analyzed by means of SDS-polyacrylamide gel electrophoresis followed by immunoblotting with anti-fibrinogen antibody. The antibody used in this study reacts with fibrinogen, fragment X, Y, D-D, D and E. The validity of this technique was confirmed by the analysis of the serum samples from patients with definite diagnosis of disseminated intravascular coagulation. Serum samples of 14 patients out of 18 with elevated FDP values and severe liver diseases were shown to contain no plasmic digest of fibrin or fibrinogen. By using the SDS-gel electrophoresis after disulfide bond reduction, seven serum samples from these 14 patients, who were shown to have no plasmic digest in serum, were found to contain unclottable fibrinogen retained in sera, while the remaining seven samples were revealed to have fibrin monomer in their sera. Four serum samples from the 18 patients were shown to have plasmic digest of fibrinogen, but these patients had additional diseases leading to intravascular coagulation.
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PMID:Analysis of fibrinogen degradation product in severe liver disorders by immunoblotting. 343 74

The present study is concerned with the formation of fibrin-fibrinogen associations in the presence of FXIIIa while fibrinolysis was inhibited by aprotinin and EACA. SDS agarose-polyacrylamide gel electrophoresis on 2.5% gels under non-reducing conditions and ultracentrifugation of the associations on urea-sucrose density gradients showed the formation of soluble cross-linked high molecular weight (HMW) fibrin-fibrinogen polymers with an estimated molecular size up to 10 times that of fibrinogen. After incubation of a mixture of 131I-fibrinogen (4 mg/ml) and 125I-desAA-fibrin (0.2 mg/ml) with FXIIIa (2 U/ml) for 1 h at 37 degrees C, about 5% of the fibrinogen and 80% of the fibrin was incorporated into the generated soluble HMW polymers. The detection of soluble crosslinked fibrin-fibrinogen polymers could be a useful diagnostic criterion for imminent DIC.
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PMID:Soluble crosslinked fibrin(ogen) polymers. 408 15

Factor VIII concentrates have been shown to have reduced ability to correct the bleeding time defect in von Willebrand's disease and to have abnormal mobility of their VIIIR:Ag on crossed immunoelectrophoresis. This report concerns the partial characterization of a fragment of VIIIR:Ag that lacks some of the normal antigenic determinants present on VIIIR:Ag. It is present in commercial factor VIII concentrates, but not in cryoprecipitate, and is recovered from the plasma of hemophilic patients who have been infused with these concentrates. The fragment is also produced during disseminated intravascular coagulation. Although it has a similar mobility on SDS agarose electrophoresis to the smallest multimer of VIIIR:Ag, they are not immunologically identical.
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PMID:Specific factor VIII-related antigen fragmentation: an in vivo and in vitro phenomenon. 618 Jul 85

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

A new method is described for the preparation of highly purified human plasminogen and plasmin with specific activity of 32 CTA units per mg of protein. With this method, the purification of the urinary plasminogen + plasmin antigenic materials from patients with chronic glomerulonephritis, disseminated intravascular coagulation syndrome and severe toxemia of pregnancy was performed, and the resulting highly purified proenzyme and enzyme were analyzed by immunoelectrophoresis, separative agar electrophoresis, gel filtration and SDS-gel electrophoresis. Our findings indicated that urinary plasmin reflects more closely the extent of intraglomerular fibrinolysis, while urinary plasminogen reflects non-selective proteinuria in patients with chronic glomerulonephritis or severe toxemia of pregnancy.
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PMID:Studies on the purification and characterization of human urinary plasminogen and plasmin. 644 89

A computer analysis of the coagulation laboratory records at the first department of Hokkaido University Hospital over a three-year period (1979-1981) was performed on 553 patients with presumptive intravascular coagulation. It is indicated that the most important diagnostic tests for DIC were Fbg, FDP, and AT III. DIC may have developed not only in patients with reduced Fbg but also in patients with normal or elevated Fbg. It is necessary to estimate the actual situations in the patients with DIC by utilizing sequential laboratory tests. In DIC, SDS-PAGE patterns of Fbg indicated the marked reduction of LMW Fbg, and the activated fibrin formation must be caused by the high affinity of thrombin for HMW Fbg. Changes in the immunoprecipitative second peak of AT III may indicate the binding of different serine proteases to AT III in DIC. Rapid and simple diagnostic tests for DIC are clinically required. An analysis of the TEG pattern using normal plasma mixed with the patient's plasma can indicate the presence of procoagulant activity in patient plasma. Such a laboratory test using TEG is the most useful and rapid diagnostic test in DIC. An anticoagulant effect of heparin therapy is determined by APTT and heparin levels. The antithrombotic effect of heparin therapy is determined by FPA as an immediate index and by Fbg, FDP, and AT III as a slow index.
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PMID:Estimation of coagulation-fibrinolytic factors in DIC. 666 45

The effects of sodium chlorate and of sodium nitrite on human erythrocytes were studied in vitro. Nitrite rapidly oxidised haemoglobin and glutathione; reduction of methaemoglobin (Hbi) by methylene blue was complete during 3 h of incubation with nitrite. With chlorate, a concentration-dependent lag phase was seen before Hbi was formed. After prolonged incubation, Hbi could no longer be reduced with methylene blue. Several other effects were observed that explain the clinical picture of chlorate poisoning which involves haemolysis followed by disseminated intravascular coagulation and renal failure: increased permeability to cations, increased resistance to hypotonic haemolysis and prolonged filtration time through polycarbonate membranes with cylindrical pores of 5 micron diameter. This suggests an increased membrane rigidity due to membrane protein polymerisation, as demonstrated by SDS polyacrylamide gel electrophoresis. Simultaneously, erythrocyte enzymes were inactivated, primarily glucose-6-phosphate dehydrogenase which is necessary for the therapeutic effect of methylene blue. This explains the inefficacy of methylene blue in the treatment of a case of chlorate poisoning that we observed (Arch. Toxicol., 48 (1981) 281).
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PMID:Erythrocyte membrane alterations as the basis of chlorate toxicity. 671 May 38

Coagulation profiles were performed in 30 consecutive alcoholic cirrhotic patients without known infection, malignancy, recent surgery, transfusion, or alcoholic intake. Hemorrhagic phenomena were present in 70% and included gastrointestinal bleeding, oozing from venipuncture sites, bruising, and epistaxis. All 30 patients had multiple liver function and coagulation abnormalities, the most frequent of which were increases in F VIII components and decreases in F XI and F VII. Also decreased in half or more of the 30 patients were Fletcher F, F II, F X, prothrombin time (PT), partial thromboplastin time (APTT), thrombin time (TT), reptilase time (RT), anti-thrombin III, and plasminogen. When comparing cirrhotic bleeders with nonbleeders, four parameters were significantly different in those with a bleeding tendency: F VII, anti-thrombin III, plasminogen, and albumin. The prolonged APTT was associated in four cases with a blocking inhibitor of unknown etiology. The prolonged TT and RT, in the absence of fibrin split products, fibrin monomers, DIC, or shortened euglobulin lysis time in any patient were suggestive of an abnormal fibrinogen, a dysfibrinogen. In three other patients, there was an inhibitor of the TT. Further investigation of the suspected dysfibrinogen in 21 patients by SDS-polyacrylamide gel electrophoresis revealed that the molecular weights of the Aalpha, Bbeta, and gamma polypeptide chains of fibrinogen were not different from normal. Two-dimensional immunoelectrophoresis of the suspected dysfibrinogen was similar to normal in 18 of 21 patients, with loss of the initial shoulder in three.
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PMID:Bleeding and coagulation abnormalities in alcoholic cirrhotic liver disease. 704 81

Sodium dodecyl sulfate-polyacrylamide gel electrophoresis utilizing a large pore gel showed that human fibrinogen (Fbg) in plasma resolved into 3 components which were tentatively designated as high molecular weight Fbg (HMW), low molecular weight Fbg1 (LMW1) and low molecular weight Fbg2 (LMW2) in order of their electrophoretic mobilities. Their estimated molecular weight were 360,000, 325,000 and 290,000 respectively. In normal plasma the ratio of HMW: LMW1: LMW2 was 71: 27: 2. Subunit chain analysis of Fbg species suggests that one of the A alpha chains in the predominant type of LMW1 is an A alpha remnant designated as A alpha', the molecular weight of which is about half that of the A alpha chain of HMW. The subunit chain formulas for the major forms of HMW and LMW1 are considered as (A alpha/1, 2)2 (B beta)2 (gamma)2 and (A alpha/1, 2) (A alpha') (B beta)2 (gamma)2 respectively. Although it is widely accepted that limited proteolysis of A alpha chain by plasmin might be the cause of Fbg heterogeneity, the conversion of HMW to LMW1 was not observed in the earliest stage of fibrinogenolysis induced by urokinase. However incubation of plasma induced the conversion of HMW to LMW1, even when t-aminomethyl-cyclohexane carboxylic acid or heparin was added to the plasma. These findings suggest that an unknown mechanism independent of plasmin or thrombin is responsible for the Fbg heterogeneity in blood. Clinically it is noticeable that the relative amount of LMW1 decreased markedly in disseminated intravascular coagulation (DIC). Animal models of DIC also exhibited essentially the same Fbg heterogeneity pattern as observed in DIC patients, when the levels of Fbg were recovering after the consumption caused by intravascular coagulation. In DIC it is considered that the consumption and compensatory production of Fbg results in the relative increase of HMW which is the freshly synthesized Fbg.
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PMID:[Studies on fibrinogen heterogeneity in disseminated intravascular coagulation]. 717 13

The soluble fibrin monomer complexes (SFMC) in 154 obstetric patients with possible disseminated intravascular coagulation (DIC) were evaluated in SDS polyacrylamide gel electrophoresis (PAGE) after precipitation with B-alanine. Other coagulation tests were performed on these patients. The patients were classified into three groups: A) patients with a clinical history of DIC (6 cases); B) patients with only the analytical alterations of DIC (35 cases); and C) patients who showed pathological obstetric diagnoses but without a clinical nor analytical history of DIC (113 cases). In the three groups, well-defined bands of less electrophoretic mobility than fibrinogen were obtained. A significant increase in the second electrophoretic band was found in group A (5.1 per cent) when compared to group C (0.5 per cent). The second electrophoretic band appeared in greater proportion in the group of patients with an unfavorable clinical evolution.
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PMID:Evaluation of the soluble fibrin monomer complexes and other coagulation parameters in obstetric patients. 717 10


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