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)

Malotilate, a hepatotropic agent, was given to 39 cirrhotic patients for more than 32 weeks. The serial changes in the serum levels of hepatic fibrogenesis markers, such as procollagen type III N-terminal peptides (P-III-N-P) and immunoreactive prolyl hydroxylase beta-subunit (IR-BPH) were analyzed. Serum albumin levels, transaminase and choline esterase activities and the Normotest values were found to be significantly improved by malotilate treatment. The levels of both serum markers of hepatic fibrogenesis were also significantly reduced by malotilate. The prognoses of the decompensated liver cirrhosis patients treated with malotilate were significantly better than those who did not receive malotilate. These results indicate that the effects of malotilate on chronic liver diseases are not simply biocosmetic, but rather are related to an improvement in the basal changes of the liver, including a decrease in the fibrogenetic stimulus. These effects of malotilate improved the prognosis of liver cirrhosis.
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PMID:Effects of malotilate treatment on the serum markers of hepatic fibrogenesis in liver cirrhosis. 285 77

Serum galactosylhydroxylysyl glucosyltransferase (S-Glu-Gal-Hyl-Tase), liver galactosylhydroxylysyl glucosyltransferase (L-Glu-Gal-Hyl-Tase), liver hydroxylysyl galactosyltransferase (L-Gal-Hyl-Tase), and liver prolyl hydroxylase (L-PH) activities were measured in rats during the development of CCl4-induced cirrhosis (0.2 ml of 33% CCl4 in light mineral oil two times weekly for 10 weeks followed by 6 weeks of no treatment). Serum and liver markers of collagen synthesis increased in a time-dependent manner reaching maximum activity at 6 weeks (S-Glu-Gal-Hyl-Tase, two times; L-PH, two times). These enzyme levels returned to normal during the 4-week recovery period. In a separate 4-week experiment, colchicine (10 micrograms/rat/day) was administered with CCl4. Colchicine prevented the increase in S-Glu-Gal-Hyl-Tase, L-Glu-Gal-Hyl-Tase, and L-Gal-Hyl-Tase induced by CCl4 and resulted in a smaller increase in L-PH. These results demonstrate that S-Glu-Gal-Hyl-Tase elevation occurs following CCl4 because of increased liver collagen synthetic activity and the hepatocellular injury produced by CCl4.
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PMID:Enzyme markers of collagen synthesis in carbon tetrachloride-induced fibrosis and during colchicine modification of CCl4-induced liver injury. 303 Jul 97

It was found that chronic intoxication of rats with ethanol results in an increase of prolyl hydroxylase activity in liver and serum of the experimental animals. The increase of enzyme activity precedes the morphological symptoms of liver damage. The possibility arises that the assay of prolyl hydroxylase in serum or in liver biopsy samples could be useful for the diagnosis of the tendency of some individuals to develop liver cirrhosis induced by ethanol.
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PMID:Prolyl hydroxylase activity as an index of liver damage induced by ethanol. 303 63

In an effort to assess connective tissue biosynthetic activity in human liver disease, collagen proline hydroxylase (a key enzyme in collagen biosynthesis) and the uptake of (35)S sulphate (a precursor of sulphated mucopolysaccharides) were measured in hepatic tissue obtained mainly by percutaneous biopsy.A procedure is described for the quantitation of collagen proline hydroxylase in cryostat sections which allows for the simultaneous histopathological examination of the liver specimen. A three to eightfold increase in the activity of this enzyme was found in four cirrhotic livers compared with the mean value of four normal livers and two biopsies from patients with Gilbert's syndrome. Elevated hydroxylase levels were found also in five patients with hepatic dysfunction but without cirrhosis (four alcoholics and one patient with persistent hepatitis associated with serum smooth muscle antibody). It is suggested that the hepatic level of collagen proline hydroxylase may be a useful quantitative index of fibroblastic activity in human liver disease. Autoradiographic studies of radioactive sulphate uptake in biopsy specimens from patients with chronic liver disease showed an exaggerated incorporation of isotope not only at sites of established fibrogenesis but also in the walls of sinusoids throughout the liver.
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PMID:Collagen proline hydroxylase activity and 35S sulphate uptake in human liver biopsies. 436 10

The activity of prolyl hydroxylase was measured in liver tissue obtained from a small series of patients with a variety of liver disease. Enzyme levels were marginally elevated in patients with fatty liver and viral hepatitis, conditions not normally associated with progressive fibrosis. In some patients with alcoholic hepatitis and in all patients with cirrhosis and chronic active hepatitis, there was a marked increase in enzyme activity. Patients with conditions characterised by high liver prolyl hydroxylase levels showed histological evidence of extensive hepatic fibrosis and also significant increases in the serum values of glutamate dehydrogenase and gamma-glutamyl-transpeptidase. Prolyl hydroxylase activity was not detected in serum.
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PMID:Hepatic prolyl hydroxylase activity in human liver disease. 625 37

Carbon tetrachloride inhalation in phenobarbitone treated rats caused a rapid rise in hepatic prolyl hydroxylase activity which was followed by an increase in hepatic collagen and free proline concentrations. Colchicine in a dose of 5 micrograms/day largely prevented the increase in hepatic collagen. This effect was not mediated by impairment of prolyl hydroxylase activity. Colchicine is of potential therapeutic value in preventing the progression of chronic liver disease to cirrhosis.
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PMID:Hepatic collagen synthesis in a rat model of cirrhosis, and its modification by colchicine. 627 60

An experimental animal model designed specifically to simulate liver fibrosis and cirrhosis in childhood is described. Phenobarbitone was administered continuously from the 4th day of life and carbon tetrachloride intermittently from the 13th day to developing rats for 10 weeks. Treated animals showed hepatic necrosis, hepatic regeneration and a progressive increase in hepatic fibrosis; cirrhosis developed before the animals reached sexual maturity at 72 days or were fully grown. Hepatic prolyl hydroxylase activity increased to a maximum level after 20 days of treatment, before increased hepatic collagen could be detected, and fell to a lower level as cirrhosis became established. Serum activities of alkaline phosphatase, aspartate aminotransferase and alanine aminotransferase gave a similar pattern, a marked increase at 20 days of age followed by a fall to near normal levels as hepatic damage became more severe. By the 26th day of life hepatic collagen levels were increased significantly and rose thereafter progressively as fibrosis became more widespread throughout the liver. Cirrhosis developed between the 38th and 75th days. Cirrhosis remained 10 weeks after discontinuation of treatment with phenobarbitone and carbon tetrachloride treatment.
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PMID:Carbon tetrachloride-induced hepatic fibrosis and cirrhosis in the developing rat: an experimental model of cirrhosis in childhood. 630 21

Total prolyl hydroxylase protein was measured in hepatic tissues of 8 patients with primary hepatocellular (PHC), 5 with acute viral hepatitis, and 5 with cirrhosis (3 alcoholic and 2 with secondary biliary cirrhosis). The mean values were compared with the mean value of 10 normal hepatic tissues. The mean values were all highly significantly elevated (P less than 0.001) in PHC, acute viral hepatitis and the cirrhotic patients, respectively. The mean L-IRPH value in PHC was about 9.50 times the control mean, while in acute viral hepatitis, and cirrhosis the mean L-IRPH values were about 3.00 and 2.30 times the control mean respectively. The mean level of L-IRPH in PHC was 4.06 times the mean level of L-IRPH in cirrhosis and 3.14 times the mean value in acute viral hepatitis. The findings of this study provide a basis for the elevated serum values of this intracellular enzyme of collagen synthesis in patients with primary hepatocellular carcinoma and the data indicate that this enzyme may be elevated to compensate for an increased rate of collagen synthesis in the malignant liver tissue.
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PMID:Liver immunoreactive prolyl hydroxylase protein in human primary hepatocellular carcinoma. 632 76

To assess whether hepatic peptidyl prolyl hydroxylase (PPH) activity could serve as a practical quantitative indicator of hepatic fibrosis or aid in the categorization, diagnosis or prognosis of hepatobiliary disorders in infancy and childhood, the activity of this enzyme has been determined prospectively by a tritium release method in 97 biopsies from 94 infants and children with the following conditions: acute hepatitis of infancy, 10 patients; extrahepatic biliary atresia, 13; previous hepatitis of infancy, 8; alpha-1-antitrypsin deficiency, 6; chronic active hepatitis, 17; chronic persistent hepatitis, 5; glycogen storage disease, 5; and 25 patients with a miscellanea of other liver disorders. PPH activity was considered in relation to diagnosis, biochemical and histological abnormality and subsequent prognosis over a 4-year period. Five liver biopsies which showed no histological abnormality were considered as "controls" having PPH values of 0.72 +/- 0.47 (mean +/- S.D.). PPH activity was significantly elevated in acute hepatitis of infancy, 9 of the 10 infants having PPH greater than 1.66 units (i.e., mean +/- 2 S.D. of the "control" value). Nine infants (70%) with extrahepatic biliary atresia also had PPH activity above this value, as did two with alpha-1-antitrypsin deficiency and 12 patients all in different diagnostic categories. PPH activity did not correlate with hepatic fibrosis as indicated by hepatic hydroxyproline concentration or by histological assessment, or with biochemical tests of liver function within any diagnostic group or in the series as a whole. PPH activity was similar in biopsies with and without histological features of cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic peptidyl prolyl hydroxylase activity and liver fibrosis--a prospective study of 94 infants and children with hepatobiliary disorders. 632 86

Four factors which stimulate collagen synthesis and prolyl hydroxylase activity in cultures of human and mouse fibroblasts have been isolated by molecular sieve chromatography from animal and human fibrotic and cirrhotic livers. These factors do not stimulate protein or DNA synthesis or total DNA in these cultures. It has also been shown that these factors, designated collagen stimulating factors F1-F4, do not owe their activity to ascorbate or glutamine. Collagen stimulating factors are heat stable, and F1 and F2 have apparent molecular weights of about 4000 and 1000 respectively. Since these factors are not present in normal animal or human liver it is suggested that they may be responsible for increased collagen production in vivo in hepatic fibrosis and cirrhosis.
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PMID:Collagen stimulating factors in hepatic fibrogenesis. 632 76


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