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 interpretation of the morphological features of alcoholic hepatitis is discussed in terms of a comparison with the results of an ultrastructural and histoenzymological study of the liver biopsies of nine patients. In these patients liver biopsies were performed in the initial stage of the illness and fifteen days after five were re-biopsied, when the clinical and biological signs were improved. The correlations between morphological and biological data were good, especially for the levels of serological and histoenzymological alkaline phosphatase and gamma-glutamyltranspeptidase evaluations. However, when histological appearances had returned to normal, after two weeks of abstinence from alcohol several histological and ultrastructural features of the initial hepatitis persisted. The presence of evolving cirrhosis was a contributing factor to the severity of the changes seen. Morphologically, apart from the changes due to chronic alcoholic intoxication (steatosis, mitochondrial alteration), the hepatitic lesions comprise Mallory's bodies, cytoplasmic oedema and mitochondrial swelling. Cholestasis was invariably present. Histo-enzymologically there was a reduction in ATPase activity suggesting a metabolic failure in the energy producing pathways. In addition, in the periphery of lobules an active cirrhotic process was present, with tubular de-differentiation of hepatocytes and an increase in gamma-glutamyltranspeptidase on the cytoplasmic membrane. Because of the absence of any topographical relationship between hepatitis and cirrhosis, the presence of lymphocytes in the neighbourhood of the ductules suggested an indirect relationship between both processes, perhaps an autoimmune response initiated by Mallory's bodies.
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PMID:[The hepatocyte in acute alcoholic hepatitis. Histoenzymological and ultrastructural analysis (author's transl)]. 3 Oct 27

The earliest and most reproduceable lesion associated with chronic alcohol abuse is fatty liver. In some alcoholics this may be superseded by alcoholic hepatitis, which may represent the link between the early lesion and cirrhosis. Alcoholic cirrhosis usually begins as a regular, monolobular variety, but is eventually transformed into an irregular, multilobular type. All stages of alcoholic liver injury have now been produced in the baboon, despite high protein and vitamin supplemented diets. Alcohol may therefore now be regarded as a direct hepatotoxin. Epidemiological studies have indicated that alcoholic liver injury begins with an intake of more than 80 g ethanol a day, and that cirrhosis is generally not seen with an intake of less than 160 g per day. The development of cirrhosis correlates with the total duration and amount of alcohol ingested. Complications of alcoholic cirrhosis include iron overload and primary hepatic carcinoma.
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PMID:Relation of alcoholic liver injury to cirrhosis. 4 93

Mononuclear-cell responses to liver extracts were studied by a migration-inhibition assay in patients with alcoholic liver disease, viral hepatitis, chronic alcoholism without evidence of liver disease, and in healthy individuals. Patients with acute alcoholic hepatitis demonstrated liver-antigen-induced inhibition of migration (migration index [M.I]equal 0-58 plus or minus 0-08, mean plus or minus S.D.), while patients with cirrhosis, alcoholism, and acute viral hepatitis, as well as healthy volunteers, did not demonstrate such a response (M.I. 0-92 plus or minus 0-13, 0-90 lus or minus 0-10, 0-86 plus or minus 0-18, 0-99 plus or minus 0-04, respectively). It is concluded that cell-mediated immunity to normal or damaged liver tissue may act to perpetuate alcoholic hepatitis and thereby contribute to the development of cirrhosis.
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PMID:Cell-mediated immunity to liver in patients with alcoholic hepatitis. 4 24

Peripheral blood and hepatic tissue T- and B-lymphocyte distributions, serum alpha fetoprotein (AFP) concentrations, and hepatic AFP were studied in 46 patients undergoing diagnostic percutaneous liver biopsy. The patients included 26 with alcoholic liver disease, 13 with nonalcoholic hepatitis or cirrhosis, and 7 with either normal histology or minor nonspecific changes. Serum AFP was determined by radioimmunoassay and hepatic tissue AFP by indirect immunofluorescence. Peripheral blood T lymphocytes were identified by the sheep red-cell rosette technique; and B lymphocytes by fluoresceinated anti-immunoglobulin antisera and IgG aggregates. Tissue identification of T lymphocytes was accomplished using an extensively absorbed rabbit antihuman thymocyte antiserum and indirect immunofluorescence; tissue B lymphocytes were identified using pepsin F (ab')2 fragments of rabbit IgG antibodies to human immunoglobulins. T lymphocytes predominanted in hepatic lymphoid infiltrates from patients with alcoholic liver disease (91+/-4%), whereas in patients with chronic active or chronic persistant hepatitis, viral hepatitis, or cryoptogenic cirrhosis proportions of T and B lymphocytic infiltrates were similar (50+/-15%). Hepatic tissue AFP was detected in 9 of 18 patients with alcoholic hepatitis; serum AFP concentration was increased in only 1 of these 9 patients. Tissue AFP was not observed in the remaining biopsy material nor were serum AFP concentrations increased. Peripheral blood T-cell numbers were significantly decreased in patients with alcoholic liver disease (P less than 0.01) and in nonalcoholic hepatitis or cirrhosis (P less than 0.025). A close relationship between peripheral blood T-lymphocytopenia and hepatic T-cell infiltrates was observed in patients with alcoholic liver disease; this relationship was less apparent in patients with nonalcoholic hepatitis or cirrhosis.
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PMID:Localization of T and B cells and alpha fetoprotein in hepatic biopsies from patients with liver disease. 5 55

Serum-25-hydroxy-vitamin-D (25 OHD) concentration has been measured in 106 patients with untreated parenchymal and cholestatic liver disease. Low mean values were found in groups of patients with alcoholic hepatitis and cirrhosis, non-cirrhotic active chronic hepatitis, lupoid and cryptogenic cirrhosis, symptomatic primary biliary cirrhosis, and acute and chronic biliary disease. In a group of patients with presymptomatic biliary cirrhosis the mean value was not significantly different from normal. It is concluded that in the presence of significant parenchymal or cholestatic liver disease serum-25-OHD concentrations are usually low. The mechanisms for the reduction remain to be clarified, but low serum-25-OHD values may play a contributory role in the aetiology of osteomalacia in chronic liver disease.
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PMID:Serum-25-hydroxy-vitamin-D in untreated parenchymal and cholestatic liver disease. 6 May 15

Studies were undertaken to evaluate the cytotoxicity of peripheral lymphocytes obtained from patients with alcoholic hepatitis. Lymphocyte cytotoxicity to Chang liver cells was investigated by a microcytotoxicity test, and that to autologous liver cells obtained by percutaneous liver biopsy was studied using a 51Cr release assay. Lymphocytes from patients with alcoholic hepatitis were found to be highly cytotoxic to Chang liver cells and autologous liver cells when compared to those of healthy subjects (P is less than 0.001). Cell-free supernatant fluid of lymphocytes from patients with alcoholic hepatitis incubated with purified alcoholic hyalin for 5 days was significantly cytotoxic to Chang liver cells (P is less than 0.01), indicating that a cytotoxic factor is elaborated by sensitized lymphocytes. A significant reduction in cytotoxicity was noted with disappearance of clinical features or direct addition of a purified isolate of alcoholic hyalin or its preincubation with lymphocytes. Preincubation of sensitized lymphocytes with acetaldehyde increased cytotoxicity for autologous liver beyond that obtained by the combined effects of lymphocytes alone and acetaldehyde alone (P is less than 0.001), interpreted as evidence that ethanol toxicity and hyperactivity of lymphocytes independently and collectively contribute to development of cirrhosis in patients with alcoholic hepatitis who continue to imbibe alcohol.
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PMID:Lymphocyte cytotoxicity in alcoholic hepatitis. 6 6

Sixteen cases of alcoholic hepatitis with alcoholic hyaline (Group I) and 13 cases without alcoholic hyaline (Group II) have been collected since 1970. These were most frequently found in the fifth decade in both groups. One female was found in Group I. Cases of about two-thirds of both groups were comsumers of 110 g or more of alcohol per day. No significant differences except fever and erythrocyte sedimentation rate were found in clinical and laboratory changes between both groups. Fatty change in liver biopsy specimens were more frequently seen in Group I than in Group II. The wedged hepatic venous pressure was markedly elevated in alcoholic hepatitis with cirrhosis and moderately elevated in alcoholic hepatitis without cirrhosis. Wedged hepatic venography showed the main portal trunk and extrahepatic collaterals, namely, reversal of the portal flow or such tendency in 2 out of 5 patients of Group I.
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PMID:Alcoholic hepatitis with and without alcoholic hyaline. 7 93

Monooxygenase enzymes are involved in the biotransformation of drugs and of environmental carcinogens. The activity of 7-ethoxycoumarin 0-deethylase and associated NADPH-cytochrome c reductase was determined in 9000 g supernatant from bioptically obtained liver specimens from patients with various liver diseases in order to study in vitro drug metabolising capacity. Monooxygenase and reductase activity was significantly higher in the livers of 21 patients with alcoholic liver disease (fatty liver, alcoholic hepatitis, cirrhosis of the liver) than in 22 normal controls or in six patients with chronic active hepatitis. The raised activity of drug-metabolising enzymes obtained from alcoholics with liver damage differs from normal values found in five alcoholics without liver disease. Both groups were comparable in respect to the amount of alcohol consumed and duration of abuse. A strikingly low monooxygenase activity was observed in eight patients with cirrhosis of the liver and ascites, with, however, no apparent effect on reductase activity. The results show that alcoholic liver disease is associated with enhanced monooxygenase and reductase activity, but alcoholism, per se, is not. This rise of drug-metabolising enzyme activity could lead to selectively increased rates of biotransformation in patients with alcoholic liver damage.
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PMID:Monooxygenase enzyme activity in alcoholics with varying degrees of liver damage. 11 58

The effects of ethanol on hepatic cellular metabolism and structure depend mainly on the dose and duration of intake. Following the ingestion of a substantial amount of ethanol, its presence alters a number of hepatic functions in part because of the change in the hepatic redox state (NADH/NAD ratio), resulting for instance in reduction of lipid oxidation. Furthermore, chronic ethanol consumption, at least in its early stages, produces adaptive metabolic changes in the endoplasmic reticulum which result not only in increased metabolism of drugs and accelerated lipoprotein production but also in activation of hepatotoxic compounds. Even more extended periods of ethanol intake result in damage to cell organelles in what can be considered a third stage of the alcohol effect namely that of injury. The injury involves primarily mitochondria, possibly as a consequence of effects of acetaldehyde, the first product of ethanol metabolism. Metabolites of ethanol also alter microtubular function. A defect in protein secretion may be the basis for protein retention and "ballooning" of the hepatocyte. Prolongation of ethanol induced injury eventually culminates in hepatic lesions such as alcoholic hepatitis and cirrhosis. Ethanol can be incriminated as a direct etiologic agent of the liver injury, since liver cirrhosis has been reproduced experimentally in baboons fed alcohol, despite an adequate diet.
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PMID:[Pathogenesis of alcoholic liver injury (author's transl)]. 11 23

The results of liver scans performed with 99mTc-sulphur colloid in 169 patients suffering from diffuse liver diseases and in 48 normal controls were evaluated. The patients with reactive hepatitis, acute hepatitis, chronic persistent hepatitis, fatty liver and fibrosis of the liver show only minimal deviations from the scintigraphic pattern. On the contrary, highly increased colloid uptake in the spleen is found in cases of chronic aggressive hepatitis, whilst the intrahepatic distribution of the colloid is approximately normal. In cases of liver cirrhosis, increased colloid uptake is found in the left lobe of the liver as well as in the spleen and in the bone marrow. Either normal findings or cirrhosis-like changes of the colloid distribution are observed in patients with alcoholic hepatitis.
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PMID:[Liver scanning in diffuse liver disease (author's transl)]. 12 69


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