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    Influence of superimposed alcoholic hepatitis on the outcome of liver transplantation for end-stage alcoholic liver disease
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    Alcoholic liver disease (ALD) is a major cause of liver-related morbidity and mortality globally, and is a chief cause of death among adults with alcohol use disorders. This chapter describes the burden, pathogenesis, diagnosis, and therapy of ALD. It also discusses the fact that alcohol abuse can be a modifying factor for other liver diseases. The chapter further discusses some hot topics such as liver transplant for patients with ALD. Alcohol abuse is one of the main causes of preventable disease worldwide. Mortality in people with alcohol use disorders is markedly higher than previously thought, particularly with women who suffer from alcohol use disorders, who generally have a higher mortality risk than men. It is indicated in patients with aggressive forms of ALD such as alcoholic hepatitis which require specific therapies (e.g. corticosteroids and/or pentoxiphylline) and in patients with other cofactors suspected of contributing to liver disease.
    Alcoholic Hepatitis
    Alcohol abuse
    Liver disease
    Alcohol and health
    Citations (15)
    Using a leucocyte migration inhibition test sensitisation to Mallory bodies (alcoholic hyalin) was found in a statistically significant 41% of 17 patients with alcoholic hepatitis. Patients with alcohol-induced fatty liver and cirrhosis did not demonstrate sensitisation. Mallory bodies are a characteristic feature of alcohol-induced liver damage, and immunological sensitisation to them might lead to liver cell death and cell progression of the hepatitis process.
    Alcoholic Hepatitis
    Liver cell
    Citations (12)
    To investigate the expression of the transforming growth factor beta 1(TGF-beta 1) mRNA in different stages of alcoholic liver disease (ALD) and its clinical value.One hundred and seven male alcoholics were grouped by clinical findings into four groups: alcohol abusers without liver impairment (n =22), alcoholic steatosis (n =30); alcoholic hepatitis (n=31); and alcoholic cirrhosis(n=24). Using peripheral blood mononuclear cells (PBMC) as samples the gene expression of TGF-beta 1 was examined quantitatively by reverse transcription polymerase chain reaction (RT-PCR) and dot blot. There are 34 healthy subjects served as control.The expression of TGF-beta 1 from all ALD patients was significantly greater than that in controls (1.320 +/- 1.162 vs 0.808 +/- 0.276, P<0.001). The differences of the expressions were significant between the patients from each groups (alcoholic steatosis, alcoholic hepatitis and alcoholic cirrhosis) and the controls (1.168 +/- 0.852, 1.462 +/- 1.657, 1.329 +/- 0.610 vs 0.808 +/- 0.276, P<0.050). No significant differences of TGF -beta 1 mRNA expression were observed between alcohol abusers without liver impairment and controls. The expressions in patients with alcoholic hepatitis and alcoholic cirrhosis were significantly greater than that in alcohol abusers respectively (1.462 +/- 1.657, 1.329 +/- 0.610 vs 0.841 +/- 0.706, P<0.050). No significant differences of TGF-beta 1 mRNA expression were observed between alcoholic fatty liver men and alcohol abusers.TGF-beta 1 expression level can be a risk factor for alcoholic liver disease and might be related to the inflammatory activity and fibrosis of the liver in patients.
    Alcoholic Hepatitis
    Steatosis
    Alcoholic fatty liver
    Hepatitis C
    Liver disease
    Citations (47)
    There are many unanswered questions in the possible autoimmune pathogenesis of alcoholic liver disease. Why do only 15-20% of chronic alcoholic patients develop alcoholic hepatitis and cirrhosis? What factors make a patient susceptible to immune events in alcoholism? What initiates immune reactivity in susceptible patients? What permits accumulation of alcoholic hyalin in patients with alcoholic hepatitis? Is alcoholic hyalin central to the pathogenesis of alcoholic hepatitis? If adducts play a role, why don't more alcoholics develop liver disease, as adducts probably form in all patients? Unfortunately, the lack of an appropriate animal model will probably allow these questions to remain unanswered for some time. However, further research into the role of adducts in alcoholic liver disease may be helpful. Isolation of adducts from hepatocytes of patients with alcoholic hepatitis may permit study of their intracellular location, formation and perhaps of their timing in the sequence of liver disease. These studies should provide additional clues to the pathogenesis of alcoholic liver disease.
    Alcoholic Hepatitis
    Pathogenesis
    Liver disease
    Autoimmune Hepatitis
    Citations (3)