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)

Heparin cofactor II (HCII) is a glycoprotein in human plasma which inactivates thrombin rapidly in the presence of heparin or dermatan sulfate. We have developed a functional assay for HCII in which inhibition of thrombin by plasma is determined in the presence of dermatan sulfate. The assay is specific for HCII by the following criteria: (a) under the conditions of the assay, 125I-thrombin forms complexes in plasma which comigrate with the thrombin-HCII complex during sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE); (b) activity detected by the assay is decreased in plasma absorbed with monospecific antibodies against HCII; and (c) purified antithrombin III (ATIII) is unreactive in the assay system. Addition of Polybrene to the assay permits determination of HCII activity in samples containing less than or equal to 12 U/mL of heparin. The range of HCII concentrations in normal individuals is 1.2 +/- 0.4 mumol/L (mean +/- 2 SD, n = 34). HCII activity was determined in 54 consecutive patients undergoing evaluation for the possibility of disseminated intravascular coagulation (DIC). Ten of the 11 patients with documented DIC had decreased HCII activity as compared with only 7 of the 43 patients without DIC (chi 2 = 19.3, P less than .0001). The concentrations of HCII and ATIII varied in parallel in most of the patients tested. A significant correlation between decreased HCII activity and decreased serum albumin concentration was also observed in these patients and in eight additional patients with hepatic failure in the absence of DIC. We conclude that HCII activity is decreased in many patients with DIC and hepatic failure.
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PMID:Heparin cofactor II activity in patients with disseminated intravascular coagulation and hepatic failure. 404 18

From the pre-natal follow-up it was remarkable that cases have been admitted relatively late. Hints to a possible development of preeclampsia could be seen from patients history or the routine check up, for example the registration of edema, fetal growth retardation and oligohydramnios. For early diagnosis of preeclampsia we recommend: Calculation of mean arterial blood pressure or its non-invasive measurement; determination of hematocrit, uric acid and total plasma protein (in particular hemorheologic measurements). Hypomagnesemia in preeclampsia, as described by some authors, was also seen in our cases. The complex symptomatology of preeclampsia could be attributed to a generalised disturbance of microcirculation, which leads to definite reactions of the organs concerned. The microcirculatory failure is caused by vasoconstriction, hemoconcentration, hyperviscosity and hypercoagulation (up to DIC and consumption coagulopathy). The resulting symptoms and syndromes can be: EPH, HELLP, hemolytic-uremic Syndrome, hepato-renal Syndrome, thrombocyte and antithrombin III deficiency etc. The drug of choice for treatment of preeclampsia is magnesium sulfate. Its application is based on long-term clinical experience and new aspects on the physiologic and pharmacologic role of magnesium. The recommendations of the German High Blood Pressure League to use calcium antagonists as a basis in the treatment of high blood pressure can be fulfilled particularly in pregnancy by the physiologic calcium antagonist Mg++. Magnesium sulfate should be given in a dosage of 24-72 g daily. The dose should also be made dependent from urinary output. Further treatment patterns of preeclampsia should be adjusted according to each case. The present results also support our hypothesis that magnesium deficiency (besides predisposing factors) could be responsible for the development of preeclampsia (present model shown in detail). Consequently, the early and long-term substitution of magnesium in pregnancy could help reduce preeclampsia.
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PMID:[Pathophysiology and clinical aspects of pre-eclampsia]. 404 84

Endotoxin administered intravenously to a group of four calves resulted in disseminated intravascular coagulation. A sublethal dose of piromen, a commercially available Pseudomonas spp endotoxin, was used. Serial measurements of total plasma fibrinogen, soluble fibrin levels, ethanol gelation tests, protamine sulfate tests, fibrinogen-fibrin-related antigen (FR-antigen) and prothrombin and thrombin times were done.Initial depression of plasma fibrinogen with a nadir of about 40% of pre-endotoxin levels at eight to 11 hours post-endotoxin (+8 to +11 hours) followed by an overcompensation to 180% at +60 to +108 hours was shown. Soluble fibrin was demonstrated in plasma from +2 to +22 hours with a peak of 100-114 mg/100 ml at +4 to +9 hours. Positive plasma ethanol gelation and protamine sulfate tests, as well as the presence of serum FR-antigen, occurred consistently following endotoxin administration. Significant increases in prothrombin times (PT) from +4 to +40 hours and in thrombin times (TT) from +4 to +16 hours were demonstrated. The peak increase of PT at +8 to +10 hours was 180%. The peak increase of TT at +6 to +9 hours was 260-290%.
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PMID:Endotoxin induced disseminated intravascular coagulation in cattle. 427 65

Three antimicrobial agents were evaluated as to their ability to neutralize the toxic effects of endotoxin in rabbits. These consisted of two cyclic polypeptides, polymyxin B sulfate and colymycin M (sodium colistimethate), and an aminoglycoside, gentamicin sulfate. Polymyxin B regularly prevented endotoxin-induced leukopenia, thrombocytopenia, and disseminated intravascular coagulation. Colymycin M had similar activity but was not as effective as polymyxin B. Gentamicin demonstrated no neutralizing ability in this study.
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PMID:Comparison between the polymyxins and gentamicin in preventing endotoxin-induced intravascular coagulation and leukopenia. 434 9

Extensive coagulation studies have been carried out on patients undergoing second trimester abortions induced by prostaglandin F2alpha. 30 patients with intraamniotic instillation of PGF2alpha have been studied and an additional 10 patients who were aborted by the extraovular route. Blood samples were obtained before onset of medication and at frequent intervals after beginning of drug administration as well as at the time of abortion. Intraamniotic administration of PGF2alpha resulted in increased levels of fibrinogen, platelets, factors 8 and 5, profibrinolysin, and fibrinolytic inhibitors during the 24 hour period after beginning of medication. The rise in the coagulation factors is suggestive of mild inflammatory process not associated with infection. Most of the indices have returned to normal levels shortly after expulsion of the fetus and placenta. Only 1 patient receiving PGF2alpha showed evidence of fibrin monomer formation as determined by protamine sulfate precipitation. Extraovular results were similar. The results have been compared to those obtained in this laboratory following hypertonic saline. With saline the results show a decrease in many factors, indicating disseminated intravascular coagulation. PGF2alpha may provide a safer method of second trimester abortion as far as the coagulation mechanism is concerned than does hypertonic saline.
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PMID:Coagulation studies during second-trimester abortions induced by PGF2alpha. 483 89

During a period of ten years ranging from January 1973 to February 1983, a total of 51 patients with primary cancer of the liver underwent hepatic resection at the Keio University Hospital. Thirty five of 51 patients were cirrhotic and two were jaundiced. Six cirrhotic patients died of liver failure within one month following hepatic resection. In order to minimize the postoperative death, it is mandatory to maintain the integrity of circulatory dynamics and microcirculation. Monitoring of circulatory dynamics with the use of Swan-Ganz catheter is very useful for managing the patients with massive transfusion, copious production of ascites and adult respiratory distress syndrome and is indispensable for hepatic resection using vascular exclusion technique. Disseminated intravascular coagulation occurs frequently after hepatic resection. It will cause hepatic failure due to microthrombi, unless prompt treatment is instituted. Score count was designed to facilitate diagnosis using platelet count, fibrinogen level, quantity of fibrin degradation product and protamine sulfate test as parameters. It is difficult to determine the optimal dose of heparin because of decreased antithrombin III and metabolism in the liver due to loss of hepatic parenchyma. Gabexate mesilate (FOY) is very effective and safe agent, since it works without antithrombin III.
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PMID:[The rationale of treatment after hepatectomy for primary cancer of the liver]. 632 52

A technique is described to completely remove antithrombin III (AT) from small amounts of human plasma by immunoaffinity chromatography on antibodies against human AT linked to Sepharose 4B. The level of heparin cofactor II (HCII) was not affected by the immunoadsorption. HCII activity was then determined by measuring the rate of human thrombin inhibition by 3 ways: a) activation with heparin in AT-free plasma, b) activation with dermatan sulfate in normal plasma and c) activation with dermatan sulfate in AT-free plasma. The normal range of HCII varied between 0.7-1.5 U/ml, as compared to a normal plasma pool containing by definition 1 U/ml. Highly significant correlations between assays as obtained from 40 normal plasmas proved the suitability of the 3 assays, although the progressive thrombin inhibition by AT, when not removed, contributed about one fifth to the thrombin inhibition by HCII in the presence of dermatan sulfate. There were also highly significant correlations between HCII activity and antigen, as determined by rocket immunoelectrophoresis using specific antibodies against HCII. Levels of HCII and AT were examined in 7 patients with hereditary AT deficiency and 7 patients with disseminated intravascular coagulation (DIC). In hereditary AT deficiency, whereas the AT activity was reduced by half, levels of HCII activity and antigen were in the normal range. In DIC, a parallel decrease of HCII and AT suggests that HCII may participate in the inhibition of thrombin released during DIC and thus provides an inhibitor reserve, once the AT level becomes subnormally low.
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PMID:Heparin cofactor II determination--levels in normals and patients with hereditary antithrombin III deficiency and disseminated intravascular coagulation. 639 34

Rapid methods for determination of fibrin-monomer complexes and fibrinogen/fibrin degradation products were studied and compared in 76 patients with different abnormalities in the hemostatic system (acute thromboses, thromboembolism of the pulmonary artery, disseminated intravascular coagulation, immune thrombovasculitis, etc). The control group consisted of 36 healthy donors. The fibrin-monomer complexes were determined by the paracoagulation tests, the ethanol test (ET) and protamin sulfate tests (PST), whereas fibrinogen/fibrin degradation products (FDP) by the staphylococcus adhesion test (SAT) in which use was made of the Newman D2S strain variety obtained by the authors. It is inferred that the ET, PST and SAT are the most suitable for use in clinical medicine, since they are accessible, simple and quick in performance. However, these tests cannot be regarded as similar or interchangeable, since they are used for studying different products of the coagulation and fibrinolytic transformation of fibrinogen.
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PMID:[Comparative study of various rapid methods of determining fibrinogen transformation products in the diagnosis of intravascular coagulation and fibrinolysis]. 647 66

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

We describe a functional assay for protein C in human plasma samples based on the ability of activated protein C to prolong the kaolin-cephalin activated partial thromboplastin time of normal plasma. Protein C is separated from its inhibitor by elution of a barium citrate precipitate, and activated by incubation with human alpha-thrombin for one hour. Thrombin is then inhibited by antithrombin III and heparin, heparin neutralized by protamine sulfate, and protein C activity measured in the partial thromboplastin time. 24 normal subjects had a mean protein C level of 94 +/- 12% (SD) of the activity in pooled normal plasma. Seven patients with severe liver disease had a mean protein C of 28%. Eleven patients with disseminated intravascular coagulation had a mean protein C of 29%. Eight patients receiving warfarin therapy had a mean protein C of 17%. The assay is relatively simple and should be suitable for general laboratory use.
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PMID:A functional assay for protein C in human plasma. 668 83


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