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)

After a short survey on the history of the therapy of liver cirrhosis the importance of the prevention of alcoholism is emphasized. A "liver diet" is regarded as unnecessary, prednisolone is recommended for the treatment of the active cirrhosis. After a short description of the principles of the therapy of biliary cirrhoses, of haemochromatosis and of Wilson's hepatocerebral degeneration the use of restriction of salt, saluretics and aldosterone antagonists in the treatment of ascites is discussed in detail. After description of the conservative therapy of the haemorrhage from varices with the compression sound, intraarterial octapressin infusion and combat against consumption coagulopathy finally the prophylaxis of the hepatoportal encephalopathy with reduction of the protein intake and the restriction of the formation of toxic products of protein metabolism in the intestine by application of neomycin or lactulose, respectively, is described.
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PMID:[Conservative therapy of liver cirrhosis]. 85 44

A specific, sensitive, and reproducible radioimmunoassay for human plasma thromboplastin antecedent (PTA, factor XI) has been developed with purified PTA and monospecific rabbit antiserum. Precise measurements of PTA antigen were possible for concentrations as low as 0.3% of that in normal pooled plasma. Normal plasma contained approximately 6 microgram PTA/ml. A good correlation (correlation coefficient 0.68) existed between the PTA procoagulant assays and radioimmunoassays among 50 normal adults (25 males and 25 females). PTA antigen was markedly reduced in plasma of 13 patients with congenital homozygous PTA deficiency (range less than 0.003-0.128 U/ml) and 9 patients with hepatic cirrhosis (0.35+/-0.17 U/ml), but was normal in those of 9 patients under treatment with warfarin, 8 patients with disseminated intravascular coagulation and 16 patients with other congenital clotting factor abnormalities, including prekallikrein deficiency (Fletcher trait) and high molecular weight kininogen deficiency (Fitzgerald trait).
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PMID:Plasma thromboplastin antecedent (PTA, factor XI): a specific and sensitive radioimmunoassay. 88 16

A secific, sensitive, and reproducible radioimmunoassay for human Hageman factor (HF, factory XII) has been developed with purified human HF and monospecific rabbit antibody. Precise measurements of HF antigen were possible for concentrations as low as 0.1% of that in normal pooled plasma. A good correlation (correlation co-efficient = 0.82) existed between the titers of HF measured by clot-promoting assays and radioimmunoassays among 42 normal adults. Confirming earlier studies, HF antigen was absent in Hageman trait plasma, but other congenital deficient plasmas, including those of individuals with Fletcher trait and Fitzgerald trait, contained normal amounts of HF antigen. HF antigen was reduced in the plasmas of patients with disseminated intravascular coagulation or advanced liver cirrhosis, but it was normal in those of patients with chronic renal failure or patients under treatment with warfarin. HF antigen was detected by this assay in plasmas of primates, but not detectable in plasmas of 11 nonprimate mammalian and one avian species.
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PMID:Radioimmunoassay of human Hageman factor (factor XII). 95 1

Endotoxins of gram-negative bacteria and of intestinal origin, insufficiently cleared by the hepatic reticulo-endothelial system are of an increasing interest within the pathogenesis of liver diseases. With purpose to obtain data concerning incidence and course of endotoxaemia in patients with liver cirrhosis an unselected group of these patients, sequentially admitted, was investigated by means of the Limulus-gelation test, regarded as most sensitive to endotoxins. At the admittance, 65% of the patients had endotoxaemia, further 14% developed endotoxaemia later. In total 79% of the patients investigated had endotoxaemia.---Bleeding from oesophageal varices was associated with endotoxaemia in 78%, functional renal impairment in 75%, consumption coagulopathy in 81%, encephalopathy in 77% and a pyrogen reaction in 82% of the patients. Regarding the Limulus assay, the dilution technique was more sensitive in detection of free endotoxaemia as opposed to the chloroform extract. It is concluded from the results that endotoxaemia in patients with liver cirrhosis is frequent and has to be viewed as relevant within the pathogeneses of chronic liver diseases.
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PMID:[Endotoxinemia in liver cirrhosis]. 96 Sep 7

The high incidence of consumption coagulopathy in active liver cirrhosis prompted us to introduce low-dosage heparin therapy (LDHT) in the management of this condition. An investigation was carried out on 109 patients with clinical and biochemical evidence of progressive liver cirrhosis, which was designed to evaluate whether in addition to basic LDHT, the administration of either vitamin K1, human fibrinogen or partial prothrombin complex (Prothromplex 500) enhanced the results obtained with LDHT alone. The normotest, PTT, thrombin coagulase activity, fibrinogen and platelet count were determined at regular intervals. A significant increase in fibrinogen and platelet count was obtained within 14 days of LDHT in about 75% of the patients and the consumption coagulopathy was halted. Additional treatment with vitamin K1 did not bring about any further increase in the prothrombin complex. Substitution therapy with factors II, IX, X and fibrinogen combined with LDHT brought the expected results. The results reported in the literature and the aims of, and indications for LDHT are discussed.
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PMID:[The therapeutic management of consumption coagulopathy in progressive liver cirrhosis: low-dosage heparin therapy (author's transl)]. 99 29

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

The effect of "low dose" heparin therapy on fibrinogen survival in patients with cirrhosis was studied in six patients. Survival of I-125 radiolabeled fibrinogen was measured using both autologous and homologous material. Average fibrinogen half-life before heparin therapy was 52 hours and after 3000 units of intravenous heparin every 6 hours was 101.8 hours. Median survival before heparin therapy was 56 hours and after therapy was 91 hours. In every instance fibrinogen survival was improved by heparin administration. These data indicate that "low dose" heparin improves fibrinogen survival in cirrhosis and suggest that disseminated intravascular coagulation is a primary process in the defibrination syndrome associated with cirrhosis.
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PMID:Fibrinogen survival in cirrhosis: improvement by "low dose" heparin. 114 42

Patients with liver disease have a variety of coagulation abnormalities. These derangements are of uncertain origin and do not always correlate with disease severity or activity. We have measured the levels and proportions of the total fibrin-related and fibrinogen-related antigens, the principal fibrin (D-dimer) and fibrinogen (D-monomer) degradation fragments and intermediates of fibrin formation (fibrin monomers) in patients with a variety of acute and chronic liver diseases in whom all known other precipitating causes of disseminated intravascular coagulation had been excluded. Fibrin-related and fibrinogen-related antigens were extracted from serum using antihuman fibrinogen-IgG covalently bound to activated amino-phenylthioether paper disks and were subjected to 4% to 11% sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Fibrin-related and fibrinogen-related antigen proportions were determined by densitometry, and their levels were measured by radioimmunoassay. Levels of total fibrin-related and fibrinogen-related antigens (and D-dimer) were significantly elevated (p less than 0.01) in patients with cirrhosis (121 to 641 ng/ml) and hepatocellular carcinoma (416 to 8,786 ng/ml) when compared with patients with acute viral hepatitis (84 to 322 ng/ml) and control subjects (38 to 186 ng/ml). In addition, D-monomer levels were elevated. These findings strongly suggest that disseminated intravascular coagulation is a component of the coagulopathy of certain liver diseases. Because fibrin-related and fibrinogen-related antigens have anticoagulant, vasoactive and immunosuppressive properties, their elevated presence may be biologically significant in these patients.
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PMID:Elevated fibrin-related and fibrinogen-related antigens in patients with liver disease. 132 11

Hemostasis is intimately related to liver function, because most coagulation factors are synthesized by liver parenchymal cells and the liver's reticuloendothelial system serves an important role in the clearance of activation products. The extent of coagulation abnormalities depends upon the degree of disturbed liver function. Acute or chronic hepatocellular diseases may display decreases in the vitamin K-dependent factors (prothrombin; factors VII, IX, and X; proteins C and S), whereas other parameters remain normal. Patients with hepatic failure may present with the entire spectrum of factor deficiencies and may even develop disseminated intravascular coagulation (DIC). Patients with liver cirrhosis have a wide spectrum of abnormalities. Except for factor VIII:C and von Willebrand factor, all procoagulant and inhibitory factors are decreased, which is a reflection of impaired protein synthesis. Abnormal fibrinogen and prothrombin molecules can be identified. Platelets are quantitatively and qualitatively altered, and most patients develop DIC. Vitamin K deficiency leads to the production of abnormal vitamin K-dependent factors. The factors lack gamma-carboxy glutamic acid residues in the NH2-terminal part of their molecules. Surgery associated with the liver leads to major hemostasis alterations. The LeVeen shunt is invariably related to DIC. Bleeding with partial liver resection is mostly mechanically induced, but chronic DIC may be present. Orthotoptic liver transplantation is associated with severe hemorrhages. These are partly due to the pre-existing hemostasis defects and partly due to DIC with a marked fibrinolytic response. This is especially noted during the anhepatic phase and when the donor liver is perfused by the recipient's blood. Postoperative recovery is quick, provided the graft is not rejected. Postoperatively, there may be an initial hypercoagulable state, which could be related to the thrombosis occasionally encountered.
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PMID:Coagulation abnormalities in liver disease. 133 67

A case of Vibrio cholerae non-O1 septicemia is described in this paper. A 45-year-old male with a three year history of liver cirrhosis, was admitted to our division with hematemesis, abdominal pain, high fever and a loss of consciousness. Three days before onset of symptoms, he traveled to Ishigaki Island and ate a raw lobster. Two days after, his temperature rose to 39.7 degrees C and the blood pressure dropped to 36/- mmHg. By endoscopic examination, an ulcer was found in the stomach, and the bleeding was stopped by electrical coagulation. Blood culture showed growth of V. cholerae non-O1. The organism was found to be sensitive to OFLX, CZX, MINO, LMOX and CP. Although DIC, infections of fungus and MRSA occurred as complications, he recovered by adequate procedures. Subsequently, he left this division after eight weeks. There are various reports related to V. cholerae non-O1 septicemia in foreign countries, but few cases have been reported in Japan. And these cases had severe underlying diseases such as leukemia and liver cirrhosis.
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PMID:[A case of Vibrio cholerae non-O1 septicemia with liver cirrhosis]. 140 1


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