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)

An assay technic for measuring heparin cofactor activity in which antithrombin activity can be assessed without plasma attenuation even in the presence of therapeutic levels of heparin is presented. Heparin-activated anti-thrombin activity was markedly depressed in plasmas of four patients with disseminated intravascular coagulation and in ten patients with cirrhosis. Residual activity in those plasmas appeared qualitatively normal, and no inhibitor (platelet factor IV activity) was observed. Plasmas from patients with disseminated intravascular coagulation and cirrhosis required more heparin to obtain in vitro clotting time prolongation equivalent to normal.
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PMID:Minimal heparin cofactor activity in disseminated intravascular coagulation and cirrhosis. 6 Aug 79

Recently it has been paid attention whether the liver diseases might induce the disseminated intravascular coagulation (DIC) or not, although it has well known that liver cirrhosis contribute to the hemorrhagic diathesis. In this paper, we studied on the hemorrhagic tendency and hemostatic tests in the patients with liver cirrhosis in order to clarify the coagulation and fibrinolytic activity. We can conclude that the hemorrhagic diathesis occurs due to the complex of decreases in platelet number, platelet functions, clotting factors, and increased fibrinolytic activity. The increased fibrinolytic activity may be primary and the frequency of clinically important DIC is quite low.
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PMID:Studies on hemorrhagic tendency in cirrhosis of the liver. 9 Jun 31

Four cases of hepatic angiosarcoma are reported with a review of 99 other cases in the English literature. Angiosarcoma of the liver is associated with chronic exposure to thorotrast, vinyl chloride, arsenicals, radium and possibly copper and with chronic idiopathic hemochromatosis. Although 40% of patients have hepatic fibrosis or cirrhosis at autopsy, the nature of the association between chronic liver disease and hepatic angiosarcoma is unknown. The clinical presentation of hepatic angiosarcoma is nonspecific with abdominal pain, weakness and weight loss common complaints and with hepatomegaly, ascites and jaundice common findings. Liver function tests are usually abnormal but there is no one liver function test or set of tests specific for the tumor. The occurrence of thrombocytopenia and disseminated intravascular coagulation is characteristic of hepatic angiosarcoma and may be related to local consumption of clotting factors and formed blood elements in the tumor. Catastrophic intraabdominal bleeding is also characteristic and occurs in one-fourth of all cases. This complication is likely related to the high incidence of clotting abnormalities and the vascular nature of the neoplasm. Selective hepatic arteriogram and open liver biopsy are the foundations of diagnostic evaluation. Percutaneous liver biopsy should be avoided. Failure to appreciate the possibility of hepatic angiosarcoma in the proper clinical setting, leading to blind percutaneous biopsy, may result in failure to make the diagnosis at the cost of significant morbidity and mortality. Survival of patients with hepatic angiosarcoma is brief; only 3% live longer than 2 years. Treatment of the tumor to date is empirical. There are probably a few patients who might benefit from radical surgery with curative intent. For all others chemotherapy is indicated. Adriamycin is active against hepatic angiosarcoma, but optimal dose and mode of administration require further investigation. Further study is also required to delineate the cause of hepatic angiosarcoma in the 60% of cases without definite epidemiologic association.
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PMID:The clinical features of hepatic angiosarcoma: a report of four cases and a review of the English literature. 36 8

Three cases of disseminated intravascular coagulation following infusion of ascitic fluid from the peritoneal cavity to the vascular system are reported in patients with hepatic cirrhosis. One of these was treated with intermittent drainage and infusion, and in the other two a LeVeen shunt was used. Studies on the ascitic fluid indicate the presence of a procoagulant material which would appear to be an activator of factor X. Preactivated factor X (Xa) from the fluid and/or a tissue factor activator of factor VII are additional possibilities.
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PMID:Procoagulant activity of ascitic fluid in hepatic cirrhosis: in vivo and in vitro. 49 63

184 autopsy cases with liver diseases were examined clinicopathologically with special reference to the incidence and distribution of microthrombi and classic thrombi in various organs. Microthrombi and/or classic thrombi were found in one or more organs in 50.0% to 59.4% of the patients with various liver diseases. But only 4 among 184 patients had many microthrombi in more than three organs and the incidence of disseminated intravascular coagulation seemed to be low in autopsy cases with liver diseases. Incidence of microthrombi showed no significant difference in the groups with and without portal vein thrombosis. Hemorrhage in the upper alimentary tracts of the patients with liver cirrhosis did not seem to develop by disseminated intravascular coagulation. Consumption of clotting factors in liver diseases seemed to occur by thrombus formation in portal vein and esophageal varices and by hemorrhage in various organs.
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PMID:Intravascular coagulation in autopsy cases with liver diseases. 50 65

Consumption coagulopathy was developed in three cases of liver cirrhosis and a case of haemophilia B upon administration of Factor IX preparations which had been tested by the manufacturers for the absence of active clotting factors according to the Japanese Minimum Requirements for Biological Products. By employing the TGT determination, however, active clotting factor(s) could be detected in some of the preparations used in these cases. Accordingly, it was found necessary to modify the current test method in the Minimum Requirements by introducing calcium ion into the test medium. There was no correlation between the clotting activitiy detected by our modified test method and the Factor IX potency of the product. Addition of heparin did not significantly influence the results in our modified method.
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PMID:A test method for the absence of thrombogenicity in factor IX complex. 54 93

The titers of components of the plasma kallikrein-kinin system have been measured conventionally by their biological functions. The functional assays are, however, antagonized by the presence of inhibitors and/or the absence of potentiators in test samples. Immunologic assays obviate these difficulties. We have developed specific, sensitive and reproducible radioimmunoassays (RIA) for HF and prekallikrein, and have applied these assays to some clinical conditions. Normal pooled human plasma contained approximately 40 microgram of HF and 50 microgram of prekallikrein per ml. RIA were able to measure concentrations of HF and prekallikrein as low as 0.1% and 0.3% that of normal pooled plasma respectively. A good correlation existed between titers measured by clotting and radioimmunoassays among 40 normal subjects (correlation co-efficient = 0.82 for HF and 0.71 for prekallifrein). There was no significantly reduced in plasmas of patients with advanced liver cirrhosis or disseminated intravascular coagulation (DIC) and in cord serums, but they were normal in plasmas obtained after strenuous physical exercise and in plasmas of patients under treatment with warfarin.
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PMID:Determination of Hageman factor (HG, factor XII) and plasma prekallikrein (Fletcher factor) by radioimmunoassays. 57 61

Testing for soluble fibrin complexes was performed using a sensitive and reliable haemagglutination assay, with red cells sensitized by fibrin monomers. The principle is based on the fact that the monomers linked to red cells and induce their agglutination. This test, used in clinical trials, has revealed the presence of soluble complexes in every confirmed case of acute DIC, but also in Chronic DIC where diagnosis is difficult to establish (negative ethanol gelation test, normal or sub-normal levels of fibrin breakdown products). In Cirrhosis of the liver, the test gives positive results in a non negligible number of cases. Several hypotheses are made to explain why in certain confirmed cases of DIC, low fibrin breakdown products levels are found.
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PMID:[The detection of soluble fibrin complexes by a haemagglutination test. Clinical applications (author's transl)]. 60 Jul 51

Affinity chromatographic studies using insolubilized fibrinogen (fibrinogen-agarose) revealed that fibrin monomer present in plasma is selectively adsorbed to fibrinogen-agarose and may be quantitatively estimated following desorption. Analysis of plasma samples from patients with myocardial infarction, cirrhosis of the liver malignant diseases and DIC confirmed the presence of considerable amounts of fibrin monomer revealing concentrations between 3 and 15 mg/100 m1 plasma as compared to normal plasma (1.96 +/- 0.37 mg/100 m1, = 27). The method is suitable for the assessment of hypercoagulable states. Standard conditions for the procedure were evaluated using 3H-labelled fibrinogen and fibrin monomer.
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PMID:Detection of thrombin-induced fibrinogen derivatives in thrombotic states. 61 80

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66


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