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)

Hepatic prolyl hydroxylase activity and collagen synthesis were measured in patients with alcoholic liver disease to determine the feasibility of using the enzyme prolyl hydroxylase as a marker of hepatic fibrogenesis. Alcoholic patients with liver histopathology consistent with normal, steatosis, alcoholic hepatitis, early cirrhosis, or advanced cirrhosis were analysed for liver prolyl hydroxylase activity and in vitro collagen synthesis. Prolyl hydroxylase activity and the rate of in vitro collagen synthesis were correlated when these parameters were measured in samples of the same liver biopsy. Mean prolyl hydroxylase activity was significantly raised in all groups of alcoholic patients with alcoholic liver disease, except those with steatosis, when compared with alcoholic patients with normal morphology. Alcoholic patients with early cirrhosis had enzyme activity (mean +/- SE: 1.367 +/-0.162 mU/mg protein) significantly raised over all other groups. Mean enzyme activity was less raised (0.985 +/- 0.097 mU/mg protein) in patients with advanced cirrhosis. The percentage of collagen synthesis in patients with early or advanced cirrhosis was also raised compared with alcoholic patients with normal morphology. Prolyl hydroxylase activity and the rate of collagen synthesis are significantly correlated (r=0.62). These findings suggest that hepatic prolyl hydroxylase activity is a useful indicator of hepatic fibrogenesis and its measurement on available liver biopsy tissue should be a potent diagnostic tool reflecting active fibrogenesis and predicting progression of alcoholic liverdisease.
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PMID:Hepatic prolyl hydroxylase and collagen synthesis in patients with alcoholic liver disease. 23 Jan 28

This paper is a speculative review of the irreversibility of cirrhosis of the liver. Experimental studies dealing with the specific issue of irreversibility of the process are summarized, and the following three general propositions are derived: 1. All experimental models of cirrhosis are reversible, provided the inciting agent is removed and sufficient time is allowed for the return to normal liver structure. 2. Experimental cirrhosis of the liver goes through two successive stages, differing (among many other features) in the time and completeness of their reversibility. 3. Increased reticulum fibers are more easily and completely resorbed than thick collagenous bundles. Human cases of cirrhosis of the liver in which the fact of regression appears to be sufficiently documented are also summarized. Most of them seem to fulfil the three conditions derived from the analysis of experimental data, namely, withdrawal of the etiologic agent at an early stage in their development (with a predominance of reticulum over collagen fibers) and allowance of sufficient time to document the disappearance of the disease. Experimental studies on the mechanisms of collagen degradation in general, and in the liver of mammals in particular, are also reviewed. It is concluded that much remains to be done but that the outcome is by no means hopeless.
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PMID:Cirrhosis of the liver: a reversible disease? 23 53

The relation between availability of free amino acids and development of cirrhosis in rat liver has been experimentally evaluated. Levels of free glycine and proline were found to increase when animals are treated with phenobarbital and carbon tetrachloride. This increase is concomitant with increase in collagen and loss of activity of enzymes responsible for degradation of amino acids. It is concluded that elevated levels of proline observed in the serum of cirrhotic patients may be a consequence, rather than a cause, of collagen accumulation in the liver.
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PMID:Cirrhosis and the synthesis of proline and glycine in rat liver. 53 2

Ultrastructural peculiarities of hepatocytes and Kupffer's cells in rats during the spontaneous reversibility of the experimental cirrhosis of the liver under the usual conditions and also under the influence of exogenous RNA, administered by different methods, were studied. The changes in cell ultrastructure proved to correlate with those of the quantitative indices of the protein synthesizing the liver function during the hepatic cirrhosis reversibility. A positive role of the RNA influence of short duration on the intracellular reparative hepatocytes regeneration, and a negative one in case of RNA influence of long duration was revealed. Participation in the resorption of collagen both of the parenchymal cells and of the stroma was shown.
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PMID:[Ultrastructural and functional features of the reversibility of sclerotic liver changes in rats treated with exogenous organ specific RNA]. 65 91

Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.
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PMID:Alcoholic hepatitis. 77 53

Using indirect immunofluorescence technique, 21 cases of hepatic cirrhosis of differing etiology were studied with type-specific antibodies to collagen type I, II, and III. In all cases the fibrous septa and portal tracts showed an increase in type III collagen. No fluorescence could be observed with antibodies to collagen type I and II. Thus, biochemical studies are supported which show, in addition to type III collagen, a new, as yet undescribed type of collagen in liver cirrhosis that is similar to type I collagen electronmicroscopically, but differs from type I collagen biochemically and immunologically. No correlation between the etiology of cirrhosis and the pattern of different collagen types could be found. The origin of different collagen types in liver cirrhosis is briefly discussed.
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PMID:[Immunohistochemical characterization of collagen in liver cirrhosis (author's transl)]. 80 1

Adult human liver biopsies were cultured from normal, alcoholic hepatitis, chronic active hepatitis, fibrosis plus alcoholic hepatitis (active cirrhosis), inactive cirrhosis, and drug hepatitis. The synthesis of collagen was estimated in cultures from 58 livers by measuring the conversion of [(14)C]proline to the [(14)C]hydroxyproline of collagen; that of glycosaminoglycans in cultures from 57 livers by the incorporation of [(3)H]acetate and (35)SO(4) into glycosaminoglycans (GAG). The synthesis of procollagen was increased only in cultures from alcoholic hepatitis, both in the pulse medium (P < 0.05) and in the chase medium (P < 0.02). The synthesis of insoluble collagen was increased in cultures from chronic (active) hepatitis (P < 0.01), fibrosis plus alcoholic hepatitis (active cirrhosis) (P < 0.001), and inactive cirrhosis (P < 0.05). Essentially all radioactive GAG was soluble in culture media. The predominant GAG were chondroitin-4 or -6-SO(4). The synthesis of GAG was increased only in cultures from fibrosis plus alcoholic hepatitis (active cirrhosis) both in the pulse medium (P < 0.01) and chase medium (P < 0.001). The data indicate that in the absence of immuno-competent cells or their secretory products, tissue cultures from livers showing biopsy evidence of active fibrosis in vivo may demonstrate increased synthesis of collagen and GAG in vitro. Increased (soluble) procollagen synthesis in cultures from alcoholic hepatitis was not associated with histologically demonstrable overt hepatic fibrosis in vivo, nor was it associated with increased GAG synthesis in vitro. No significant difference was demonstrable in collagen or GAG synthesis in paired cultures which contained either 300 mg/dl ethanol or 3.75 mg/dl methylprednisolone compared to their respective controls.
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PMID:The rate of synthesis of glycosaminoglycans and collagen by fibroblasts cultured from adult human liver biopsies. 87 75

Hypercholesterolemia was induced in rats by feeding them a high cholesterol olive oil diet. The livers were homogenized in modified Krebs-Ringer medium and centrifuged at 35,000 x g. The supernatants from livers of both hypercholesterolemic and normal rats were found to stimulate collagen synthesis in freshly isolated embryonic chick-tendon fibroblasts. However, this was significantly greater in the supernatants from fatty livers. The stimulating principle proceed to be dialyzable, non-lipid and heat-stable. There were at least two factors involved, the more effective of which was trypsin-sensitive, with a molecular weight below 2,000. The results suggest that a mediator is formed in the livers of hypercholesterolemic rats which might be responsible for the enhanced collagen synthesis of fibrotic processes vivo, e.g., in atherosclerosis and liver cirrhosis.
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PMID:Factors stimulating collagen synthesis from the livers of hypercholesterolemic rats. 94 25

This study was designed to determine whether prolonged ingestion of alcohol in combination with a nutritious diet can produce hepatic cirrhosis in the rat. Male Wistar-strain rats were fed a high protein liquid diet in which alcohol comprised 35.5% of total calories. Rats maintained on this diet for 19 months had normal growth. There was no evidence of cirrhosis after 19 months. Histological examination showed no hepatocellular necrosis, inflammation, or increased connective tissue. Ultrastructural study showed no substantial changes, except for occasional mitochondrial enlargement in cells containing increased lipid. Biochemical analyses at 19 months showed moderate increase in hepatic triglyceride levels and slight increase in hepatic collagen content in the experimental groups.
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PMID:Minimal hepatic changes in rats fed alcohol and a high casein diet. 94 87

Histologic findings in liver biopsy specimens obtained from 88 patients before and one and two years after end-to-end jejunoileal bypass are compared. In addition to the expected fatty changes, mild changes of centrilobular, pericellular fibrosis were present in the initial biopsies in 8.6%; a year later they had become apparent in 46%. Portal-central bridging developed in 6.8%, and early micronodular cirrhosis in 3.4%--always in those with central pericellular fibrosis. Electron-microscopic study of pre-bypass liver biopsies from eight addtional patients showed collagen and electron-dense material resembling basement membranes within the spaces of Disse in seven, although only four had light-microscopic evidence of minimal central pericellular fibrosis. The existence of these light- and electron- microscopic changes before jejunoileal bypass suggests that there is a lesion in morbid obesity that may be exacerbated during the first year after operation.
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PMID:Hepatic lesions of central pericellular fibrosis in morbid obesity, and after jejunoileal bypass. 97 Mar 70


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