Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assay of serum antigens related to the aminoterminal propeptide of type III procollagen has been suggested for monitoring fibrotic processes in the liver. These antigens were measured here in 61 alcoholics who were divided into four groups on the basis of liver histology: normal light microscopy, fatty liver, alcoholic cirrhosis with hepatitis, and inactive cirrhosis. All the subjects having alcoholic hepatitis with cirrhosis had elevated values in the assay, whereas some of those with either fatty liver or inactive cirrhosis still had normal values. It was, therefore, not possible on the basis of this method alone to distinguish fatty liver from cirrhosis or alcoholic hepatitis, although very high values were suggestive of alcoholic hepatitis. In a follow-up study, the aminopropeptide value decreased slowly during recovery from alcoholic hepatitis and increased rapidly after a new drinking bout. The antigens detected by the assay are heterogeneous in human serum. The proportions of the three main peptide forms varied during recovery from alcoholic hepatitis, the authentic propeptide being the main one at the acute stage, but almost disappearing later. The usefulness of the assay could probably be improved if distinct assays were available for the different antigen forms.
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PMID:Aminoterminal propeptide of type III procollagen in serum in alcoholic liver disease. 660 26

Alcoholic liver disease has been shown to progress even after cessation of ethanol intake and the involvement of an immunological mechanism has been suggested. To study whether lymphocyte cytotoxicity for autologous human hepatocytes is involved in the pathogenic process of alcoholic liver disease, hepatocytes (target cells) obtained by a needle liver biopsy from 36 patients with alcoholic liver disease were isolated by enzymatic digestion and incubated with autologous peripheral lymphocytes (effector cells). Using a microcytotoxicity assay, a cytotoxic effect was observed in patients with active cirrhosis or alcoholic hepatitis, but not in those with inactive cirrhosis, hepatic fibrosis or fatty liver. When lymphocytes were separated into T cell enriched and non-T cell enriched fractions, this cytotoxic effect was significantly greater with the non-T cell enriched lymphocyte fraction than with the T cell enriched fraction. The addition of aggregated IgG reduced the cytotoxic effect of the lymphocytes. These results suggested that antibody-dependent cell-mediated cytotoxicity may be of pathogenic importance in alcoholic liver disease.
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PMID:Lymphocyte cytotoxicity for autologous human hepatocytes in alcoholic liver disease. 660 8

The frequency of serum autoantibodies including anti-albumin antibodies was investigated for patients with various categories of alcoholic liver disease (ALD). The 95 patients were grouped into 3 categories: fatty liver (25 cases), alcoholic hepatitis (29 cases), and alcoholic cirrhosis (41 cases), and each group was matched with healthy controls by age, sex, ethnic origin and socio-economic status. For all patients with ALD, there was a 5-fold greater frequency over the controls of positive tests for antinuclear antibody (ANA), but titres were low; the pattern of ANA reactions was speckled in 50% of the cases. For patients with alcoholic cirrhosis, there was an 8-fold increase in frequency over the controls in anti-smooth muscle antibody (ASMA), but titres were low, pointing to a possibility that autoimmunity might be one of several determinants of progression of alcoholic hepatitis to cirrhosis. For none of the groups was there an increase over the controls in the mean titre of sheep red cell agglutinins, nor were there increased haemagglutinin titres of antibody to bovine serum albumin or to human albumin, arguing against a general increase in antibody production in ALD. Greater knowledge of the frequency, significance and pathogenicity of reactive autoantibodies which occur in response to various types of tissue damage is required for interpretation of the increase in ANA and ASMA in alcoholic liver disease.
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PMID:Autoantibodies, sheep cell agglutinins and anti-albumin antibodies in alcoholic liver disease. 660 35

Acetaldehyde dehydrogenase (ALDH) activity in liver biopsy specimens was considerably reduced in alcoholic cirrhosis (n = 5), elevated in alcoholic fatty liver (n = 11)--probably due to enzyme induction--only slightly elevated in alcoholic hepatitis (n = 6), but unaffected in non-alcoholic liver diseases (n = 23) in comparison with specimens obtained from patients with minimal liver lesions. We will argue as a working hypothesis that alcoholics with induced ALDH activity will mainly develop fatty liver, whereas reduced hepatic ALDH appears to be a reason for elevated acetaldehyde levels followed by additional liver injury and progression at least for alcoholic cirrhosis.
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PMID:Aldehyde dehydrogenase (E.C. 1.2.1.3) in chronic alcoholic liver diseases. 662 3

Plasma, obtained just prior to diagnostic liver biopsy in 71 patients with various liver diseases, was examined by electroimmunoassay using immunoglobulin against human fibronectin and purified plasma fibronectin as standard. The plasma fibronectin concentration was not significantly different from age- and sex-matched healthy controls in patients with chronic persistent or chronic active hepatitis (n = 7), primary biliary cirrhosis (n = 8), alcoholic fatty liver (n = 9), alcoholic hepatitis (n = 10), and alcoholic cirrhosis (n = 16). Patients with acute viral hepatitis (type A (n = 2); type B (n = 7); type non A, non B (n = 1] had significantly (P less than 0.01) raised plasma fibronectin concentrations (median 506 mg/l (range 339-804] compared to controls (median 399 mg/l (range 304-462]. Morbidly obese patients with fatty liver (n = 11) had significantly (P less than 0.001) raised plasma fibronectin concentrations (median 610 mg/l (range 429-862] compared to controls (median 361 mg/l (range 303-419].
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PMID:Plasma fibronectin concentrations in patients with liver diseases. 665 70

The role of the Ito cells in perivenular and intralobular scarring in alcoholic liver disease was examined morphologically. There was a substantial decrease in the number of Ito cells in the midzone of the hepatic lobule in both fatty liver and alcoholic hepatitis as judged by light microscopy. By electron microscopy, however, an increase in "activated" Ito cells or a few fibroblasts were found in small foci of fibrosis in association with inflammation and hepatocellular degenerative changes in most cases of alcoholic hepatitis. Cytoplasmic protrusions of activated Ito cells extended to the hepatocytes undergoing degenerative changes including Mallory body formation. There was an apparent transition from Ito cells to activated Ito cells and to fibroblasts. It is suggested that Ito cells may play a role in perivenular and intralobular fibrosis in alcoholic hepatitis.
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PMID:The role of the Ito cell in perivenular and intralobular fibrosis in alcoholic hepatitis. 668 40

Since alcoholism is a major health problem, mechanisms responsible for various forms of alcoholic liver disease (e.g., fatty liver, alcoholic hepatitis, and cirrhosis) require elucidation. Knowledge of these mechanisms is needed to provide a sound framework to treat alcoholic liver disease, to prevent its occurrence and to identify those most susceptible to it. Israel and co-workers proposed that ethanol-induced necrosis results from hypoxia to centrilobular hepatocytes as a consequence of an alcohol-induced increase in hepatic oxygen utilization (Y. Israel, H. Kalant , H. Orrego , J. M. Khanna , L. Videla , and J. M. Phillips, 1975, Proc. Natl. Acad. Sci. USA, 72(3), 1137-1141). We have employed several new techniques to evaluate this hypothesis. Procedures have been developed to make measurements of hepatic metabolism within the hepatic lobule in the isolated, perfused liver using miniature light guides and oxygen electrodes. By comparing these lobular measurements to global metabolism and to hepatic morphology determined by light and electron microscopy, a coherent, quantitative description of lobular oxygen metabolism is emerging. With these techniques, the lobular oxygen gradient was measured directly in isolated, perfused rat livers. This gradient was elevated in livers from ethanol-treated rats, an effect which was blocked by the antithyroid drug, propylthiouracil. Restriction of oxygen delivery to the isolated liver produced stable, circumscribed zones of virtual anoxia localized around the central vein. Anoxic stress led within minutes to centrilobular injury with complete sparing of periportal areas. Cellular injury was characterized by the formation of membranous blebs on the surface of centrilobular hepatocytes. When hypoxic tissue was reoxygenated , blebs were released into the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is hypoxia involved in the mechanism of alcohol-induced liver injury? 672 87

Ethanol was found to be capable to stimulate the microsomal xenobiotic-metabolizing enzyme system of human liver. However, this effect was seen only in cases of alcoholic liver damage (fatty liver, alcoholic hepatitis). Alcoholics without alcoholic liver injury had enzyme activities comparable to control patients, who had no liver disease. On ethanol abstinence the enzyme stimulation was reversible within 20 days. Stimulation of xenobiotic-metabolizing enzyme activity in alcoholic liver disease seems to be related to ethanol induced toxicity. The highest enzyme activities were observed in patients on enzyme inducing drugs (2- to 6 fold increase), whereas in alcoholic liver disease enzyme activities were doubled. These results suggest that the stimulation of the microsomal enzyme system caused by ethanol is different from the enzyme induction seen on inducing drugs.
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PMID:[Foreign substance-degrading enzyme system of the human liver. Modification by alcohol, other exogenous factors and liver diseases]. 679 Mar 94

Thickening around the terminal hepatic venule (THV) in alcoholics has been implicated as a marker for fibrosis and cirrhosis. To test this hypothesis, we evaluated 107 liver biopsy specimens from patients with normal liver histologic features (12), fatty livers (30), mild alcoholic hepatitis (15), and florid alcoholic hepatitis (29). Twenty-one follow-up liver biopsy specimens from patients with fatty liver and alcoholic hapatitis were also available for this study. Two observers (S.M.N., V.H.N.) graded 18 histologic features on a scale of 0 to 3. There was no significant difference in the prevalence of THV thickening in normal biopsy specimens and in various forms for alcoholic liver injury. There was also no correlation between the degree of THV thickening and steatosis, necrosis, or inflammation. Thickening of the THV was most common in the presence of lobular and subsinusoidal fibrosis. Cirrhosis developed in nine of ten alcoholic patients who had subsinusoidal and lobular fibrosis. These findings illustrate that the marker for progressive fibrosis and development of cirrhosis is lobular and subsinusoidal fibrosis and not the isolated thickening of the THV.
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PMID:Importance of terminal hepatic venule thickening. 689 54

Excessive alcohol ingestion results in profound derangements of lipid and lipoprotein metabolism, reflecting the effects of ethanol on peripheral and hepatic lipid metabolism and its toxic effects on hepatic function. The alterations in plasma lipids and lipoproteins are secondary to complex abnormalities of lipoprotein synthesis, secretion and catabolism. The major effects of alcohol include fatty liver secondary to excessive triglyceride synthesis, resulting in an imbalance between synthesis and hepatic secretion; hypertriglyceridemia and hypercholesterolemia; defective plasma cholesterol esterification; and decreased high-density lipoprotein cholesterol. In patients with severe alcoholic hepatitis, the plasma lipoproteins have an abnormal structure and apoprotein composition. Although these changes are usually reversible with abstinence from alcohol (if liver function returns to normal), they indicate serious effects of alcohol on the liver, which may culminate in cirrhosis and hepatic insufficiency. These effects of alcohol on lipids and lipoproteins should be contrasted with the elevation in high-density lipoprotein cholesterol concentration produced by moderate alcohol intake and the possibility that this increase may protect against the development of atherosclerotic disease.
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PMID:Lipid and lipoprotein abnormalities in alcoholic liver disease. 702 Sep 88


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