Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assay of Kininase II activity in the serum of 92 jaundice patients revealed a significant difference between the group with viral hepatitis (268.48 +/- 70.93 U/ml), that with biliary obstructions (133.05 +/- 37.64 U/ml) and with cirrhosis (173.76 +/- 79.56 U/ml). The increase encountered in patients with medical jaundice correlates well with total bilirubinaemia but not with cytolysis enzymes. This suggests failed demolition of ACE by the hepatocyte during cellular stress.
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PMID:[Variations in serum kininase II activity in acute jaundice]. 301 14

Hyaluronan (hyaluronic acid) is a linear polysaccharide formed from disaccharide units containing N-acetylglucosamine and glucuronic acid. It is ubiquitously distributed in the organism but is found in the highest concentrations in soft connective tissues. The molecular weight of hyaluronan is usually in the order of 10(6) to 10(7). Due to hydrogen bonding, the chain is rather stiff and the molecule behaves in solution as an extended, randomly kinked coil. Molecules of hyaluronan start to entangle already at concentrations of less than 1 g/l and form a continuous polymer network. Some of the functions of the polysaccharide have been connected with the unique physical chemical characteristics of the network such as its rheological properties, flow resistance, osmotic pressure, exclusion properties and filter effect. Hyaluronan is synthesized in the cell membrane by adding monosaccharides to the reducing end of the chain. The precursors are UDP-glucuronic acid and UDP-N-acetylglucosamine. The polysaccharide grows out from the cell surface and it can be shown that fibroblasts, for example, surround themselves with a coat of hyaluronan. The rate of biosynthesis is regulated by various factors, such as growth factors, hormones, inflammatory mediators, etc. The responsible enzyme, hyaluronan synthase, is a phosphoprotein and the regulation of the synthetic rate is apparently via phosphorylation. The hyaluronan is at least partly carried by lymph flow from the tissues. Part of the material is taken up and degraded in the lymph nodes. Another part is carried to the general circulation and taken up in the endothelial cells in the liver sinusoids. These cells have specific receptors for hyaluronan, which also recognize chondroitin sulphate. The uptake in the liver of high-molecular weight hyaluronan is very efficient and its normal half-life in serum is only in the order of 2 to 5 min. The polysaccharide is rapidly degraded in the lysosomes to low-molecular weight products, lactate and acetate. The total turnover of hyaluronan in serum is in the order of 10-100 mg/24 h. The normal concentration of hyaluronan in serum is less than 100 micrograms/l with a mean of 30-40 micrograms/l. High serum levels have been noted in liver cirrhosis (impaired uptake in the liver) and rheumatoid arthritis (increased synthesis in the tissues). Hyaluronan has been shown to interact specifically with certain proteins and cell surfaces. It binds to proteoglycans in cartilage and other tissues and fills an important structural role in the organization of the extra-cellular matrix.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemistry of hyaluronan. 312 95

In 15 patients with cirrhosis of the liver and 10 control subjects, 7.5 mmol sodium propionate and 7.5 mmol sodium acetate were instilled endoscopically into the duodenum. Venous concentrations of propionate and acetate were measured for 90 min after administration of the enteral dose by gas-liquid chromatography. In patients with liver cirrhosis, propionate rose from a basal value of 6.1 +/- 4.7 (SD) microM to a peak concentration of 50.1 +/- 25.6 microM, whereas, in controls, it rose only from 1.4 +/- 1.6 to 10.3 +/- 7.6 microM. The oral propionate clearance was significantly lower in patients with cirrhosis (4.51 +/- 1.63 L/min) than in controls (118.47 +/- 154.79 L/min). Acetate went up from 39.5 +/- 16.3 to 134.1 +/- 62.7 microM in patients with cirrhosis and from 60.9 +/- 19.0 to 102.0 +/- 44.0 microM in controls. The oral acetate clearance was lower in patients with liver cirrhosis (2.80 +/- 2.17 L/min) than in control persons (10.86 +2- 5.72 L/min). The differences between the groups were more striking for propionate than for acetate values. It is concluded that the systemic availability of propionate and acetate is higher in patients with liver cirrhosis than in controls. This may be due to portosystemic shunting and/or diminished hepatic and extrahepatic extraction of the acids.
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PMID:Systemic availability of propionate and acetate in liver cirrhosis. 339 88

The single dose kinetics of (Z)-(3-methyl-4-oxo-5-piperidino-thiazolidin-2-ylidene)acetate (etozolin) and its active metabolite ozolinone were determined in 6 healthy volunteers, in 12 patients with acute hepatitis and in 15 patients with hepatic cirrhosis with ascites. In hepatitis, the elimination half-life of etozolin was 4 times longer resulting in a 2 fold rise in the AUC. At the same time, plasma levels of ozolinone were lower and consequently the AUC of his metabolite was reduced. In cirrhosis, the plasma level time curves of etozolin and ozolinone differed significantly from the controls and also from those of the patients with acute hepatitis. For etozolin Cmax was reduced to about 1/2, the elimination half-life being increased by a factor of 5. This resulted in a 3 fold higher AUC. As for ozolinone the reduction of plasma levels was more pronounced--Cmax fell to 1/6 of the control value--so that in spite of a longer elimination half-life, the AUC fell to 1/2. Ascites concentrations of etozolin and ozolinone were almost identical to the plasma concentration. The results suggest that acute hepatitis and hepatic cirrhosis lead to a reduced formation of ozolinone. As a result, etozolin accumulates and plasma levels of oxolinone drop. Moreover, both substances enter the ascites to a significant degree. It is concluded that these changes in the kinetics of this lipophilic diuretic do not allow a reliable dosage regimen in patients with hepatic cirrhosis and ascites.
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PMID:Altered kinetics of etozolin and its active metabolite ozolinone in hepatitis and hepatic cirrhosis with ascites. 344 68

The material from 113 point liver biopsies was studied. In 11 biopsy samples hepatic cirrhosis of viral origin was diagnosed, in 15 there was an alcoholic cirrhosis of the liver, and in 23--primary biliary cirrhosis. The comparative group included 8 patients with CPG, 13 with CAG, 32 with alcohol induced fatty dystrophy and 12 with non-alcoholic fatty dystrophy. Twenty six biopsy samples in which there were no inflammatory changes, the hepatic structure was unaltered, were used as controls. Stellate reticuloendotheliocytes were identified by means of acid-alpha-naphthyl-acetate esterase test. Quantitative assessment of stellate reticuloendotheliocytes (SR) was made stereometrically. In cases of primary biliary cirrhosis (PBC), active viral and alcoholic cirrhosis significant SR activation was found (due to hepatic parenchyma necroses) to maintain homeostasis. The biggest SR activation was revealed in PBC which is connected with the involvement of the immune mechanisms in this disease.
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PMID:[Stellate reticuloendotheliocytes in cirrhosis of the liver]. 359 4

Net acetate uptake/release by various tissues was studied in vivo in fed, starved and Paromomycin-treated rats and in patients with cirrhosis of the liver. In humans the portal vein, hepatic vein and hepatic arterial blood flow rates were determined simultaneously. In rats acetate is only intestinally produced and released into the portal vein. Intestinal production is decreased by 33% in starved and Paromomycin-treated rats compared to fed animals. Portal vein hepatic vein acetate differences are linearly related to the portal vein acetate concentration (r = 0.92). Acetate uptake from the portal vein by the liver was found when the portal venous concentration exceeded 180 mumol l-1. In humans the hepatic net acetate uptake from the portal vein/net acetate release into the hepatic vein, measured as mmol min-1, is linearly related to the portal vein acetate concentration (r = 0.96). The data indicate that the liver may homeostatically regulate the systemic acetate concentration in rat and man.
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PMID:Role of gastrointestinal tract and liver in acetate metabolism in rat and man. 393 Feb 58

Desmopressin acetate 0.3 microgram/kg was given intravenously to nine patients with chronic liver disease and to a further six such patients in a double blind controlled study versus placebo. Desmopressin acetate significantly shortened the bleeding time compared with basal values in both groups and compared with placebo. There was also a significant decrease in partial thromboplastin time (but not prothrombin time) and significant increases in factor VIII and its components, von Willebrand factor and ristocetin cofactor activity, but not in factors VII, IX, X, XI, or XII. Increased fibrinolysis could be blocked by concomitant administration of tranexamic acid. No important side effects were seen. The multimer pattern of von Willebrand factor was studied for the first time in chronic liver disease. It was normal, but after administration of desmopressin acetate the percentage of multimers of higher molecular weight increased significantly. This may be an important mechanism in the shortening of the bleeding time in cirrhosis, as has been shown in uraemia and other conditions after administration of desmopressin acetate. Desmopressin acetate may be useful in correcting defects in primary haemostasis in chronic liver disease.
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PMID:Desmopressin and bleeding time in patients with cirrhosis. 393 77

A model system utilizing a highly purified partially desialylated thyroxine-(T(4)) binding protein (STBG) was studied. STBG was prepared by the same affinity chromatographic method we have reported for preparation of highly purified T(4)-binding globulin (TBG). The necessary prerequisite for preparation of STBG was the use of T(4)-substituted Sepharose which had been repeatedly exposed to large volumes of serum for purification of TBG. STBG moved more slowly on cellulose acetate electrophoresis than TBG but had the same molecular weight and antigenic determinants as TBG. It bound T(4) with a 1: 1 molar ratio but its affinity for T(4) was about 10 times less than that of TB. STBG had about onefourth the sialic acid content of TBG and the electrophoretic mobility of this protein was similar to that of a T(4)-binding protein with a mobility slower than that of TBG which has been seen in the electrophoretic patterns of some normal human serums and in serums of patients with hepatic cirrhosis and which does not appear to be an artifact caused by storage and freezing of serum. This fourth slowly migrating T(4)-binding region in electrophoretograms of cirrhotic serums is completely abolished by prior incubation with rabbit antiserum to TBG. The in vitro production of partially desialylated TBG from T(4)-Sepharose which had been previously exposed to large volumes of serum may be due to adsorption of neuraminidases to the Sepharose either directly from serum or as the result of bacterial contamination. Partial desialylation of TBG in vivo may be an early step in the catabolism of this protein.
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PMID:Studies on human thyroxine-binding globulin. VI. The nature of slow thyroxine-binding globulin. 411 56

Plasminogen and plasmin have been determined in the same plasma samples in normal subjects and in various physiological and pathological conditions (pregnancy, liver cirrhosis, untreated cancer, and myocardial infarction during treatment with streptokinase) by means of two different methods. These were an enzymatic assay and a new immunochemical assay based on radial immunodiffusion employing cellulose acetate strips.A significant correlation was found in normal subjects. However, in the other conditions marked discrepancies were observed in the results by the two methods. These findings might be related to variations in the functional activity of plasminogen and plasmin in disease.
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PMID:Enzymatic and immunochemical determination of plasminogen and plasmin in different physiological and pathological states. 425 95

Cytocentrifuged preparations of mononuclear cells in blood and pleural fluid were stained for acid alpha-naphthyl acetate esterase (ANAE) in order to characterize the lymphocytes of pleural effusions histochemically. The cellular samples were obtained from 42 patients with pleural effusions caused by tuberculosis, pneumonia, cancer, malignant lymphoma, sarcoidosis, congestive heart failure, hepatic cirrhosis or nonspecific causes. The mean percentage of ANAE-positive lymphocytes from patients with tuberculous pleural effusion was significantly greater (P less than 0.001) in pleural fluid (85.6%) than in peripheral blood (70.0%). Tuberculous pleural fluid also contained a higher mean percentage of ANAE-positive lymphocytes than did pleural fluid from patients with cancer (75.0%), malignant lymphoma (50.0%), pneumonia, nonspecific disease (74.9%) or transudates (59.3%). The findings show that ANAE staining is useful for demonstrating T lymphocytes in pleural effusions. The pathogenetic role of these T lymphocytes and the diagnostic significance of demonstrating ANAE-positive cells in pleural effusions are discussed.
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PMID:Acid alpha-naphthyl acetate esterase staining of lymphocytes in pleural effusions. 617 49


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