Disease relevance of Liver Diseases, Alcoholic

• We compared the presence of serologic markers of hepatitis B virus (HBV) infection with the presence of the viral DNA in the livers of patients with alcoholic liver disease with or without hepatocellular carcinoma [1].
• Eighty-two other patients were excluded because they had multiple transfusions, hemophilia, intravenous drug use, human immunodeficiency virus infection, hepatitis B infection, hemochromatosis, or alcoholic liver disease [2].
• It is proposed that porphyria cutanea tarda results from the combination of an inherited defect in uroporphyrinogen decarboxylase and an acquired factor, usually siderosis associated with alcoholic liver disease [3].
• Final diagnoses, based on synthesis of clinical and laboratory data, included (a) primary hemochromatosis (n = 25; 19 homozygous, 6 heterozygous); (b) secondary hemochromatosis (n = 7); (c) alcoholic liver disease (n = 11); (d) chronic active hepatitis (n = 3); and (e) other (n = 2) [4].
• We compared PIIIP measurements and PGA index in patients with various histological forms of alcoholic liver disease (104), primary biliary cirrhosis (38), and chronic B virus hepatitis (27), and in healthy age-matched controls (30) [5].

Psychiatry related information on Liver Diseases, Alcoholic

• This study demonstrates that, although rare in Caucasians, possession of the mutant c2 allele of CYP2E1 increases the risk of alcoholic liver disease at a given level of cumulative alcohol consumption [6].
• The purpose of this study was to clarify the role of polymorphism of these ethanol-metabolizing enzymes in drinking behavior and the progression of alcoholic liver disease among Japanese men [7].
• We propose that carnosine (which is remarkably nontoxic) or related structures should be explored for possible intervention in pathologies that involve deleterious aldehydes, for example, secondary diabetic complications, inflammatory phenomena, alcoholic liver disease, and possibly Alzheimer's disease [8].

High impact information on Liver Diseases, Alcoholic

• After consuming comparable amounts of ethanol, women have higher blood ethanol concentrations than men, even with allowance for differences in size, and are more susceptible to alcoholic liver disease [9].
• Amiodarone hepatotoxicity simulating alcoholic liver disease [10].
• The mean uroporphyrinogen decarboxylase activity was lower in liver from seven male patients (9.0 pmol of coproporphyrin per minute per milligram of protein) than in 12 controls, including seven with alcoholic liver disease (22.3 pmol per minute per milligram; P less than 0.05) [11].
• By contrast, TNF-alpha was detected at low levels in liver biopsies from normal individuals or patients with alcoholic liver disease and low expression of TNF-alpha mRNA was observed in these specimens [12].
• The role of liver in the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) was studied in normal subjects and patients with alcoholic liver disease by measurement of thyrotrophin (TSH) and total and free T4 and T3 in randomand serial serum samples [13].

Chemical compound and disease context of Liver Diseases, Alcoholic

• In the present study it was investigated whether circulating antibodies from patients with alcoholic liver disease recognize acetaldehyde-liver protein adducts [14].
• Thromboxane inhibitors attenuate pathological changes in alcoholic liver disease in the rat [15].
• The role of polymorphism in manganese superoxide dismutase in susceptibility to alcoholic liver disease [16].
• CONCLUSIONS: Antibodies from alcoholic cirrhotics specifically recognized hydroxyethyl radical-cytochrome P4502E1 adducts, suggesting the possible implication of these antigens in the development of autoimmune reactions in alcoholic liver disease [17].
• Nitric oxide production in experimental alcoholic liver disease in the rat: role in protection from injury [18].

Biological context of Liver Diseases, Alcoholic

• Altered furosemide pharmacokinetics in chronic alcoholic liver disease with ascites contributes to diuretic resistance [19].
• Enhanced cyclooxygenase-2 gene expression in alcoholic liver disease in the rat [20].
• Continuing hepatic injury despite cessation of ethanol intake has suggested a potential role for altered humoral and cellular immunity in the pathogenesis of alcoholic liver disease [21].
• To clarify the pathogenetic role of acetaldehyde in the development of alcoholic liver disease, genotyping of aldehyde dehydrogenase-2 genes was performed and the clinical features of the alcoholic liver disease patients with different genotypes were compared [22].
• Thus a progressive and selective depletion of mitochondrial glutathione is demonstrated in the liver in this experimental model of alcoholic liver disease and associated with mitochondrial lipid peroxidation and progression of liver damage [23].

Anatomical context of Liver Diseases, Alcoholic

• Mitochondrial GSH depletion by ethanol feeding preceded the onset of functional changes in mitochondria, suggesting that mitochondrial GSH is critical in maintaining a functionally competent organelle and that the greater depletion of mitochondrial GSH by ethanol feeding in PV cells could contribute to the pathogenesis of alcoholic liver disease [24].
• Thyroid hormones in alcoholic liver disease. Effect of treatment with 6-n-propylthiouracil [25].
• It is believed that production of acetaldehyde, and the increase in the redox-state of hepatocytes, are responsible for many of the dysfunctions associated with alcoholic liver disease [26].
• GRO alpha levels correlated with IL-8 levels and were higher in patients with alcoholic liver disease and parenchymal neutrophil infiltration [27].
• Antibodies to microfilaments were found frequently in sera from patients with chronic active hepatitis (67%) and primary biliary cirrhosis (53%) but were rare in sera from patients with alcoholic liver disease (25%) and in control sera (3%) [28].

Gene context of Liver Diseases, Alcoholic

• Genetic polymorphism of ADH2/ALDH2 in patients with alcoholic liver disease was not different from that of alcohol dependents [29].
• In this study, we examined the expression of IFN-alpha signaling components and its inhibitory factors in 9 alcoholic liver disease (ALD) and 8 healthy control liver tissues [30].
• Mallory bodies (MBs) are cytoplasmic inclusions that contain keratin 8 (K8) and K18 and are present in hepatocytes of individuals with alcoholic liver disease, nonalcoholic steatohepatitis, or benign or malignant hepatocellular neoplasia [31].
• CONCLUSIONS: Serum MCP-1 concentrations are raised in alcoholic liver disease and reflect severity of hepatic inflammation [32].
• A study of HLA-A and B antigens in 248 patients with biopsy diagnosed alcoholic liver disease was conducted to examine for a genetic predisposition to alcohol related liver injury [33].

Analytical, diagnostic and therapeutic context of Liver Diseases, Alcoholic

• Plasma levels of nonconjugated estrone (E1), estradiol-17beta (E2), and estriol (E3) and excretion of these estrogens in urine in conjugated and nonconjugated forms were measured by radioimmunoassay in 17 healthy males and 33 males with alcoholic liver disease [34].
• Effect of an intravenous infusion of ethanol on serum enzymes and lipids in patients with alcoholic liver disease [35].
• A group of patients in an intensive care unit with alcoholic liver disease (known to elevate angiotensin-converting enzyme) and a low free thyroxine index had depressed angiotensin-converting enzyme levels (16.9 +/- 1.5 U/mL, p less than 0.01) [36].
• A multicentered trial using uniform scoring criteria such as the Alcohol Prognosis Scale is needed to better define the selection of patients with alcoholic liver disease and long-term outcome of alcoholism after transplantation [37].
• Thus, in this new animal model of alcoholism, ethanol feeding produced the features of alcoholic liver disease concurrent with hepatic deficiency of selected nutrients [38].

References