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)

alpha 1-Acid glycoprotein, an acute phase reactant synthesised by the liver, has been reported to be increased in neoplastic conditions and reduced in chronic liver disease. We measured serum alpha 1-acid glycoprotein by a nephelometric method in 186 subjects (112 males, 74 females): 55 had mild chronic liver disease (chronic hepatitis and steatofibrosis), 45 cirrhosis, 38 hepatocellular carcinoma, 15 extra-hepatic malignant disease; 33 healthy subjects were used as controls. Analysis of variance demonstrated a significant variability among groups (F = 17.08, P = 0.0000). Higher concentrations of alpha 1-acid glycoprotein were detected in malignant extra-hepatic disease than in all other groups (P < 0.01); concentrations of alpha 1-acid glycoprotein were higher in hepatocellular carcinoma than in cirrhosis (P < 0.01). Multiple regression analysis by groups (dependent variable = alpha 1-acid glycoprotein; group 1 = mild chronic liver disease + cirrhosis; group 2 = hepatocellular carcinoma) showed a significant correlation for both group 1 (r = 0.6264, F = 8.005, P = 0.0000) and group 2 (r = 0.8947, F = 13.643, P = 0.0000). The significant standardised regression coefficients were: cholinesterase, C-reactive protein, gamma-glutamyltransferase and iron (negative) for regression upon group 1; C-reactive protein, alpha 1-antiproteinase, gamma-glutamyltransferase, iron (negative) for regression upon group 2. A difference between the 2 regression equation coefficients was detected (F = 5.209, P = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase of serum alpha 1-acid glycoprotein despite the decline of liver synthetic function in cirrhotics with hepatocellular carcinoma. 810 7

Hepatic cirrhosis is the end stage in chronic liver diseases and this condition cause the patient's death because of hepatic failure. A prognosis of patients with hepatic cirrhosis depend on the liver function, especially the function of mass of residual hepatocytes and this function expressed by level of serum albumin, cholinesterase (Ch E) or ICGR-15. This function is improved a management of nutrition because hepatocytes are regenerate by intake of protein. In compensated hepatic cirrhosis, hepatocytes are regenerate by dietary intake of 100-120 g/day of protein and the function of mass of residual hepatocytes is increased. The prognosis of these patients with compensated hepatic cirrhosis are improved by this management of nutrition.
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PMID:[The managements of nutrition for hepatic cirrhosis]. 811 93

Hypersplenism is defined as the association of anemia, leukopenia, or thrombocytopenia with bone marrow hyperplasia and splenomegaly. Hypersplenism is common in liver cirrhosis and frequent in patients with portal hypertension. The effects of portacaval shunt are variable; hypersplenism hardly ever improves but rarely develops after surgery. Since the spleen is a major component of the mononuclear phagocyte system, splenectomy reduces antibody synthesis. Although splenectomy abolishes hypersplenism, it may lead to sepsis. Recently, partial splenic embolization, using gelform injected directly into the splenic artery, has been performed in patients with cirrhosis. Partial splenic embolization induces an increase in the number of circulating blood cells. In addition, the levels of albumin, hepaplastintest, cholesterol and cholinesterase are increased significantly after treatment. Partial splenic embolization rarely causes problems and may actually be beneficial.
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PMID:[Hypersplenism in liver cirrhosis]. 811 16

Ten healthy patients and 25 patients with cirrhosis of the liver (10 Child's A, 10 Child's B and 5 Child's C) received a bolus dose of mivacurium chloride 150 micrograms kg-1. The electromyographic response was monitored throughout anaesthesia until recovery of the first twitch of the train-of-four (TOF) (T1/T0) to at least 85% and the TOF ratio (T4:T1) to at least 80%. There was no significant difference between the two groups in the onset of neuromuscular block, but recovery was prolonged in the cirrhotic group compared with the healthy patients (respective mean times to recovery of T1/T0: to 5% = 20.2 vs 11.2 min (P < 0.05); to 10% = 23.8 vs 13.4 min (P < 0.005); to 25% = 28.4 vs 16.6 min (P < 0.005); to 50% = 41.1 vs 20.1 min (P < 0.005); to 75% = 43.8 vs 24.9 min (P < 0.005). Recovery of T4:T1 to 70% = 48.1 vs 27.4 min (P < 0.005)). Recovery was most prolonged in the Child's C patients. Mean plasma cholinesterase activity was less in the cirrhotic compared with the healthy group (mean 582 (SD 254) iu litre-1 vs 1125 (303) iu litre-1) (P < 0.001) and there was a significant negative correlation between plasma cholinesterase activity and all the indices of recovery (P < 0.001 for all except recovery index (P < 0.01)). We conclude that patients with hepatic cirrhosis may be sensitive to mivacurium, which could be explained, at least in part, by the lesser plasma cholinesterase activity.
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PMID:Pharmacodynamics of mivacurium chloride in patients with hepatic cirrhosis. 812 97

Plasma myeloperoxidase levels in patients with cirrhosis were compared with those in patients with chronic hepatitis and healthy controls by means of a specific radioimmunoassay for myeloperoxidase. The mean concentration of plasma myeloperoxidase in cirrhotic patients (309.1 +/- 17.2 ng/ml, n = 41) was markedly higher than that in chronic hepatitis patients (222.6 +/- 17.2 ng/ml, n = 21) (p < 0.01) and normal controls (219.5 +/- 5.7 ng/ml, n = 50) (p < 0.01). Plasma myeloperoxidase showed good negative correlations with neutrocyte count (r = -0.32, p < 0.01), thrombocyte count (r = -0.40, p < 0.01), red blood cell count (r = -0.32, p < 0.01), serum albumin (r = -0.35, p < 0.01), and cholinesterase (r = -0.32, p < 0.02) and positive correlations with serum alkaline phosphatase (r = 0.49; p < 0.01) and lactate dehydrogenase (r = 0.31, p < 0.01) in patients with cirrhosis or chronic hepatitis. Among lactate dehydrogenase isozymes, a good positive correlation was seen between plasma myeloperoxidase and lactate dehydrogenase-2 (r = 0.40, p < 0.01) and lactate dehydrogenase-1 (r = 0.03, p < 0.02). Plasma myeloperoxidase was significantly higher in the cirrhotic and chronic hepatitis patients with splenomegaly (341.1 +/- 19.4 ng/ml, n = 31) than in those without splenomegaly (217.4 +/- 12.2 ng/ml, n = 29) (p < 0.01). We also examined the difference between plasma levels of myeloperoxidase in the portal and peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High plasma concentration of myeloperoxidase in cirrhosis: a possible marker of hypersplenism. 824 62

The glutathione (GSH) S-transferases are believed to have dual functions as hepatic detoxifying enzymes and intrahepatic binding proteins. Little is known about their alterations in human liver diseases. Therefore, we have studied the relationship between the enzyme activity and rose bengal (RB) binding in hepatic cytosol and plasma indocyanine green (ICG) kinetics in patients with various liver diseases. The enzyme activity was measured in samples of hepatic cytosol obtained from 52 patients. In addition, the content of cationic and neutral transferases was estimated in 17 biopsy samples by densitometry of Coomassie blue stained sodium dodecyl sulphate polyacrylamide gel electrophoretograms. RB binding studies also were performed on cytosol samples. ICG kinetic parameters were determined using the two-compartment open model in 17 patients who were given the dye (0.5 mg kg-1) intravenously. Correlations between the enzyme activity and liver function tests, content of the enzyme, RB binding and ICG kinetic parameters were evaluated. The following results were obtained. (1) The enzyme activities were high in alcoholic liver disease, fatty liver and Gilbert's syndrome, and low in cirrhosis. (2) The enzyme activities were positively correlated with serum cholinesterase activity, serum albumin level and hepaplastin test, and negatively correlated with ICG retention rate at 15 min. (3) The enzyme activity, its content and RB binding affinity of the cytosol were positively correlated with each other. (4) The enzyme activity was positively correlated with hepatic ICG distribution volume. These results are consistent with the role of the GSH S-transferases as ligandins in intracellular storage of dyes.
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PMID:Relationship between content of hepatic glutathione S-transferases and the kinetics of indocyanine green elimination in various liver diseases. 825 11

Serum cholinesterase (ChE) (E.C. 3.1.1.8) is a glycoprotein which has 36 potential sites of asparagine-N-linked sugar chains. The structures of oligosaccharides released from ChE on hydrazinolysis were studied by serial lectin affinity column chromatography, exoglycosidase digestion, and methylation analysis. Seventy-three % of the sugar chains occurred as biantennary oligosaccharides and the remainder as C-2 and C-2,4/C-2,6 branched tri- and tetraantennary oligosaccharides. Several percentages of the Lewis X antigenic determinant and fucosylated mannose core were linked to them, and their sialic acid residues were linked to nonreducing terminal galactose residues at the C-3 and C-6 positions. Aleuria aurantia lectin-reactive ChE with the Lewis X antigenic determinant increased in hepatocellular carcinomas and liver cirrhosis compared with chronic hepatitis; on the other hand, Aleuria aurantia lectin-reactive ChE did not change significantly after transcatheter arterial embolization and was not related to the serum levels of alpha-fetoprotein and carcinoembryonic antigen in patients with hepatocellular carcinomas. Accordingly, the analysis of Aleuria aurantia lectin-reactive ChE is clinically useful for differentiating liver cirrhosis from chronic hepatitis and to identify high risk groups for hepatocellular carcinomas, i.e., cirrhotic patients in Child's A grade.
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PMID:Increase of fucosylated serum cholinesterase in relation to high risk groups for hepatocellular carcinomas. 826 62

When compared to 32 healthy normal weight normolipidemic control subjects, plasma protein C antigen and serum cholinesterase activity were significantly decreased in 17 patients with decompensated cirrhosis of the liver and in 29 critically-ill surgical patients displaying the acute phase reaction, most of them without evidence of consumption coagulopathy. The low levels of these variables are considered to be subsequent to impaired and dysregulated hepatic protein synthesis. On the contrary, plasma protein C and serum cholinesterase were increased in 20 nephrotic patients and in 20 overweight hypertriglyceridemic subjects, a finding highly suggestive of enhanced hepatic synthesis probably related to an accelerated turnover of triglycerides. A discrepancy between low serum cholinesterase activity and normal or even high plasma protein C antigen was noted in 15 patients with cholestasis. This was particularly evident in 7 subjects with extrahepatic cholestasis and an abnormal pattern of hepatic protein synthesis or impaired clearance of plasma protein C would appear to develop in such pathological conditions.
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PMID:Clinical studies on plasma protein C. Correlation with serum cholinesterase. 829 22

We measured serum erythropoietin (EPO) immunoenzymatically in 245 subjects (151 male, 94 female) to investigate the pathophysiology of its liberation in patients with liver disease. Twelve patients had acute hepatitis, 60 mild chronic liver disease (CLD), 50 cirrhosis (CIR), 43 hepatocellular carcinoma (HCC), 16 malignant extrahepatic disease, 32 benign extrahepatic disease (BEN); 32 subjects served as healthy controls. Higher EPO levels were found in all groups of patients as compared with controls (Bonferroni's test, P < 0.01); CIR and HCC had higher values than CLD and BEN (P < 0.01). By multiple regression analysis, EPO correlated with haematocrit, cholinesterase and C-reactive protein (F = 18.63, P < 0.0001). Thus, circulating EPO increases in patients with liver disease, particularly in its more advanced forms. Besides anaemia, both impairment of liver function (possibly via decreased EPO metabolism) and inflammation seem to play contributory roles in elevating serum EPO.
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PMID:Evidence for a multifactorial control of serum erythropoietin concentration in liver disease. 755 88

We studied 608 consecutive cases of anti-HCV-positive chronic liver disease. In 358 patients the diagnosis was established by needle liver biopsy. In 250 patients with liver cirrhosis the diagnosis was made on the basis of the unequivocal clinical signs and the results of imaging procedures. Chronic HCV infection is usually observed in adults or elderly patients; the age of the patients steadily increases with the progression of the illness to the more severe stages. Jaundice was infrequent in patients with chronic hepatitis or early cirrhosis; clinical symptoms and laboratory tests are of little value in differentiating CPH from CAH or in detecting early cirrhosis. Serum aminotransferases were usually only slightly elevated in all stages of the disease. Despite the mildness of the hepatic cytolysis, the progressive reduction in serum cholinesterase and albumin concentrations and the progressive increase in the serum alkaline phosphatase activity indicate progressive failure in the hepatic function in the course of the illness. The histological study showed that steatosis, follicular portal inflammation and eosinophilic changes in the hepatocytes were prominent features of chronic HCV infection. In contrast, severe piecemeal necrosis without bridging was rarely observed.
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PMID:Clinical and histological aspects of chronic HCV infection and cirrhosis. 840 7


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