Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess whether the hepatitis C virus plays an important role in Chinese patients with acute and chronic liver disease, antibodies to HCV (anti-HCV) were measured by enzyme immunoassay in 67 patients with type A and B acute viral hepatitis, 165 patients with non-A, non-B (NANB) hepatitis, 438 patients with chronic hepatitis, 200 patients with postnecrotic liver cirrhosis, 72 patients with alcoholic liver disease, 55 patients with non-alcoholic fatty liver, 24 patients with toxic and drug-induced hepatitis, and 20 patients with other chronic liver diseases. Anti-HCV was not detected in sera from patients with type A and B acute viral hepatitis, toxic and drug-induced hepatitis, primary biliary cirrhosis, Wilson's disease, or lupoid hepatitis. The anti-HCV prevalence was found to be highest in patients with NANB hepatitis (59% in sporadic and 73.2% in transfusion-associated), 16.4% in non-alcoholic fatty liver, 5.6% in alcoholic liver disease, 6.8% in chronic hepatitis, and 16% in postnecrotic liver cirrhosis. In patients with chronic hepatitis, the anti-HCV prevalence was significantly higher in HBsAg-negative (15/34, 44.1%) than in HBsAg-positive cases (15/404, 3.7%; P less than 0.0001). The results indicate that HCV is a major agent of NANB hepatitis and plays an important role in HBsAg-negative chronic liver disease in Taiwan.
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PMID:Prevalence of anti-HCV among Chinese patients with acute and chronic liver disease. 131 64

Malondialdehyde (MDA) level was determined spectrophotometrically with thiobarbituric acid method on 50 healthy persons and 160 patients with alcoholic and nonalcoholic liver diseases. Alcoholics without liver damage show normal plasma MDA values. Alcoholic fatty liver, alcoholic hepatitis and alcoholic liver cirrhosis cause an increase of MDA values. The highest concentrations of MDA were found on patients with acute virus hepatitis. Also noninfectional hepatitis and nonalcoholic liver cirrhosis showed an elevated MDA-Level. Liver damage and lipid peroxidation are considered as closely connected processes.
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PMID:[Malondialdehyde concentration in blood plasma of patients with liver diseases]. 164 26

Serum DNA polymerase activity (DNA-P) was detected in 27.6 per cent of non-A, non-B (NANB) hepatitis patients, 8.7 per cent of patients with alcoholic liver disease (ALD), 8.6 per cent of hepatitis B surface antigen (HBsAg)-positive patients and 19.0 per cent of HBsAg-negative blood donors with elevated serum glutamic-pyruvic transaminase (SGPT) concentrations. In contrast, none of the patients with hepatitis A, drug-induced liver injury or non-alcoholic fatty liver had DNA-P in their sera in the acute phase of the illness. All HBsAg-positive samples with detectable DNA-P were strongly positive for hepatitis B virus (HBV) DNA, but the samples from patients with NANB hepatitis and ALD and HBsAg-negative blood donors had no HBV DNA. Sensitivity to actinomycin D showed the heterogeneity of DNA-Ps in HBsAg-negative blood donors; the enzyme activity of one type was inhibited by 100 micrograms/ml of actinomycin D, whereas the other was not. The preference for exogenous template primers of these DNA-Ps was different to those of HBV and human retroviruses. The results reveal the prevalence of serum DNA-P in NANB hepatitis patients and suggest that two distinct agents are relevant to the aetiology of NANB hepatitis.
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PMID:Prevalence and heterogeneity of serum DNA polymerase activity in patients with non-A, non-B hepatitis and HBsAg-negative blood donors with elevated SGPT. 212 73

The role of endotoxin in the pathogenesis of progressive liver disease is receiving increasing attention, but remains controversial. Similarly, although alcoholic hepatitis is now recognized as the transitional link between alcoholic fatty liver and advanced alcoholic liver disease, the aetiology of liver cell necrosis in alcoholic hepatitis is not known. Rats fed a nutritionally adequate liquid alcohol diet according to the formula of Lieber and DeCarli developed fatty livers. Littermates fed an identical diet and challenged with small IV doses (1 microgram/g body weight) of E. coli lipopolysaccharide endotoxin (LPS) developed focal necrotizing hepatitis. Control littermates fed an identical calorie balanced but alcohol free diet and challenged with identical doses of LPS did not develop any liver lesions. The hepatocyte necrosis with associated inflammatory changes induced by LPS in fatty livers has some features of early human alcoholic hepatitis and suggests that progressive alcohol induced damage may be multifactorial in origin.
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PMID:Endotoxin induced hepatic necrosis in rats on an alcohol diet. 330 47

Circulating antibodies reacting specifically with hepatocytes isolated from ethanol pretreated rabbits have been demonstrated by two techniques - induced cytotoxicity and immunofluorescence. In the cytotoxicity assay antibodies were found in seven of 19 (39%) of patients with alcoholic fatty liver (with or without fibrosis), six of 13 (46%) of those with alcoholic hepatitis, 15 of 36 (43%) of those with cirrhosis, and seven of 14 patients (50%) of those with hepatitis and cirrhosis. In the immunofluorescence studies, nine of 15 sera induced a granular pattern of fluorescence on the ethanol pretreated hepatocytes; two sera which induced significant cytotoxicity did not induce immunofluorescence. No ethanol related antibodies were found in normal individuals or in patients with other types of acute or chronic liver disease. These results show that antibodies directed against ethanol altered liver cell determinants are present in the serum of 43% of patients with alcoholic liver disease, and suggest a mechanism whereby chronic alcohol consumption may, by inducing antigenic changes in hepatocyte membranes, trigger a cell damaging immune reaction.
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PMID:Antibodies to alcohol altered liver cell determinants in patients with alcoholic liver disease. 619 63

Ethanol is easily absorbed from the intestine and diffuses quickly throughout body water. The bulk of ethanol is metabolized in the liver, where alcohol dehydrogenase, a complex mixture of isoenzymes, oxidizes ethanol to acetaldehyde. Ethanol abuse produces functional and structural changes in the gastrointestinal tract, such as in the stomach, small intestine, liver, and pancreas. Accumulating evidence suggests direct toxicity of ethanol and possibly of acetaldehyde. Fatty liver, alcoholic hepatitis, liver cirrhosis, acute and chronic gastritis, deranged structure and function of the small intestine, acute and chronic pancreatitis, and pancreatic lithiasis are some of the sequelae of ethanol abuse. Recent investigations have enhanced our understanding of the functional and structural changes of the gastrointestinal tract produced by the abuse of ethanol.
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PMID:Ethanol, the liver, and the gastrointestinal tract. 719 92

Caffeine elimination was studied in 419 patients with cirrhotic and noncirrhotic liver disease of different etiology (hepatitis B virus infection n = 79; hepatitis NANB virus infection n = 74; ethanol-induced liver damage n = 143; primary biliary cirrhosis I-IV n = 63; cryptogenic liver cirrhosis n = 60) following oral administration of 366 mg caffeine. Caffeine clearance in the control group was 69 +/- 33 ml/min (age-matched healthy volunteers and patients without liver disease). Caffeine clearance in acute hepatitis B (70 +/- 60 ml/min) chronic persistent hepatitis B (81 +/- 56 ml/min), chronic aggressive hepatitis B (107 +/- 66 ml/min), posthepatitic liver cirrhosis B (84 +/- 62 ml/min), acute hepatitis NANB (94 +/- 69 ml/min), chronic persistent hepatitis NANB (122 +/- 60 ml/min), chronic aggressive hepatitis NANB (87 +/- 52 ml/min) and posthepatitic cirrhosis NANB (59 +/- 26 ml/min) is not reduced in comparison with controls. In patients with alcoholic fatty liver (127 +/- 71 ml/min, p < 0.05) caffeine clearance is enhanced, in alcoholic hepatitis (57 +/- 72 ml/min) comparable to controls and in alcoholic cirrhosis reduced (36 +/- 44 ml/min, p < 0.05). In primary biliary cirrhosis I-IV caffeine clearance is higher than in controls (117 +/- 59 ml/min, p < 0.05). In cirrhotic liver disease of different origin caffeine clearance is inversely related to the serum bilirubin level. However, the absolute value is determined in addition by the underlying disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine elimination in cirrhotic and non-cirrhotic liver disease of different etiology. 748 16

Morphological changes in liver biopsies from 40 alcoholic patients were studied, 20 of which being ordinary alcoholics (40-80g ethanol/day) and the other 20 being heavy drinkers (above 80g ethanol/day for over 20 years). All being male who have neither type B nor type C hepatitis. The basic morphological changes observed being: 1. Liver cell degeneration including fatty degeneration & focal ballooning, decrease in liver cell size, occasional giant mitochondrion and Mallory's body formation. 2. Focal necrosis with neutrophil infiltration. 3. Pericellular fibrosis of liver cells, hepatic fibrosis and early cirrhosis. Alcoholic liver disease can be divided into 5 types: I. alcoholic fatty liver (AFL), II. alcoholic hepatitis (AH), III. alcoholic hepatic fibrosis (AHF), IV. alcoholic liver cirrhosis (ALC), V. slight alcoholic liver disease (SALD). The degree of liver damage (liver cell necrosis and hepatic fibrosis) is closely related to the amount of daily ethanol intake. The progression of liver damage observed in our study is much milder than reports from Europe, the U.S. and Japan.
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PMID:[Morphological study on 40 cases of alcoholic liver disease]. 804 54

We measured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employees, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcoholic liver cirrhosis, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 +/- 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 +/- 5.1 and 13.7 +/- 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and gamma-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics.
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PMID:Serum carbohydrate-deficient transferrin as a marker of alcohol consumption in patients with chronic liver diseases. 848 62

Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver, n = 8; hepatitis, n = 13; liver cirrhosis, n = 9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing 125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of 125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78,000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.
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PMID:Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases. 896 93


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