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)

The authors examined the action of D-penicillamine on the ultrastructure of hepatocytes and the condition of the base substance in the rat's liver, with experimental CCl4-cirrhosis. (D-penicillamine was given to these rats during 4 and 6 months). It was discovered that the using of D-penicillamine on the early stages of experiment (until 4 months) reduced the process of the development of the liver cirrhosis. This fact was confirmed by the reducing of the level of base substance in the liver and reducing of the quantity of collagen in the Disse space, as well as by the absence of fibres in the intercellular spaces near sinusoid. When the D-penicillamine was given longer the increasing of the beta-NAG activity with simultaneous severe reducing of the GAG and destruction of hepatocyte's organelles in the experimental rat to the 6 months of experiment were observed. The authors consider that these data are the evidence of the negative effect of the long using of D-penicillamine in the stage of decompensated cirrhosis of the liver.
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PMID:[Effects of D-penicillamine on the ultrastructure of hepatocytes and state of the base substance in the liver of rats with experimental cirrhosis]. 233 8

Chronic liver diseases are characterized by an increase in connective tissue components in liver tissue. The determination of Col 1-3 peptide of type III procollagen (P-III-P) in serum of patients seems to be a useful parameter of hepatic fibroplasia. Specific radioimmunoassays are available for Col 1-3 (P-III-P) and the Col 1 and Col 1-3 (P-III-P-Fab) peptides of type III procollagen and for laminin P1 fragment. These proteins and the activity of N-acetyl-beta-glucosaminidase (beta-NAG) were measured in 94 patients with chronic liver diseases, and in 74 healthy controls. In addition, direct immunofluorescence studies were done for laminin P1 in normal and fibrotic liver tissues. In normal human liver, laminin was found in the basement membrane of bile ducts and in blood vessel walls. In fibrotic liver tissue, laminin additionally occurred in periportal areas and in sinusoids co-distributed with other connective tissue components. In serum concentrations of P-III-P, P-III-P-Fab and laminin were higher in patients than in healthy subjects. Laminin concentration was increased in early stages of chronic liver disease, possibly as a marker of regeneration; the highest concentrations were in active cirrhosis and chronic active hepatitis. The determination of P-III-P and P-III-P-Fab provided information on synthesis and degradation of type III collagen: In inactive cirrhosis, Col 1 peptide was increased in relation to Col 1-3 peptide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of serum laminin P1, procollagen-III peptides, and N-acetyl-beta-glucosaminidase for monitoring the activity of liver fibrosis. 269 3

Two methods of inducing liver cirrhosis in the rat were studied. Intragastric administration of CCl4 for 16 weeks according to Proctor and Chatamra was compared to the administration of thioacetamide in the drinking water (0.3 g/l) for the same period. CCl4 administration induced micronodular cirrhosis in 6/8 animals with a 27% mortality. Thioacetamide induced cirrhosis in 6/8 animals without mortality. The histologic pictures differed somewhat in that the CCl4 group exhibited more necrosis and cellular swelling while the thioacetamide group had more nuclear atypias and proliferation. Biochemically both groups had elevated plasma levels of aspartate aminotransferase. The lysosomal enzyme beta-hexosaminidase (beta-NAG) showed a transient increase in the thioacetamide animals, while beta-glucuronidase decreased. CCl4-induced cirrhosis led to an increase in beta-NAG. Plasma zinc decreased in both groups as well as liver zinc content in the CCl4 group, while there was a continuous elevation of liver zinc in the thioacetamide group. We conclude that oral administration of thioacetamide is a simple and reliable method of inducing experimental liver cirrhosis. The differences in histological appearances and some biochemical parameters may be caused by the different mechanisms of action of thioacetamide and CCl4.
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PMID:Thioacetamide- and carbon tetrachloride-induced liver cirrhosis. 276 88

Some urinary enzymes (NAG, AAP, lysozyme) considered to be sufficiently sensitive and reliable markers of renal damage were controlled in 20 patients with cirrhosis of the liver and in 20 healthy control subjects. The results, stated as mean +/- SD, showed a statistically very significant increase (p < 0.01) of NAG and lysozyme in cirrhotics. Furthermore, this increase could be at least in part related with the seriousness of clinical condition. On the basis of these results, we think the urinary dosage of NAG and lysozyme is, in the subjects with liver cirrhosis, a bloodless method to show an early renal damage.
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PMID:[Urinary enzymes in liver cirrhosis: useful early markers of renal damage?]. 791 12

The role of urinary biomarkers of kidney injury in the prediction of adverse clinical outcomes in acute renal failure (ARF) has not been well described. The relationship between urinary N-acetyl-beta-(D)-glucosaminidase activity (NAG) and kidney injury molecule-1 (KIM-1) level and adverse clinical outcomes was evaluated prospectively in a cohort of 201 hospitalized patients with ARF. NAG was measured by spectrophotometry, and KIM-1 was measured by a microsphere-based Luminex technology. Mean Acute Physiology, Age, Chronic Health Evaluation II (APACHE II) score was 16, 43% had sepsis, 39% required dialysis, and hospital mortality was 24%. Urinary NAG and KIM-1 increased in tandem with APACHE II and Multiple Organ Failure scores. Compared with patients in the lowest quartile of NAG, the second, third, and fourth quartile groups had 3.0-fold (95% confidence interval [CI] 1.3 to 7.2), 3.7-fold (95% CI 1.6 to 8.8), and 9.1-fold (95% CI 3.7 to 22.7) higher odds, respectively, for dialysis requirement or hospital death (P < 0.001). This association persisted after adjustment for APACHE II, Multiple Organ Failure score, or the combined covariates cirrhosis, sepsis, oliguria, and mechanical ventilation. Compared with patients in the lowest quartile of KIM-1, the second, third, and fourth quartile groups had 1.4-fold (95% CI 0.6 to 3.0), 1.4-fold (95% CI 0.6 to 3.0), and 3.2-fold (95% CI 1.4 to 7.4) higher odds, respectively, for dialysis requirement or hospital death (P = 0.034). NAG or KIM-1 in combination with the covariates cirrhosis, sepsis, oliguria, and mechanical ventilation yielded an area under the receiver operator characteristic curve of 0.78 (95% CI 0.71 to 0.84) in predicting the composite outcome. Urinary markers of kidney injury such as NAG and KIM-1 can predict adverse clinical outcomes in patients with ARF.
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PMID:Urinary N-acetyl-beta-(D)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure. 1726 47