Antioxidants versus corticosteroids in the treatment of severe alcoholic hepatitis—A randomised clinical trial
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Alcoholic Hepatitis
Clinical endpoint
Prednisolone
Alcoholic Hepatitis
Liver disease
Hepatitis C
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Alcoholic Hepatitis
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To investigate whether complement pathway activation contributes to the clinical and histological features of acute alcoholic hepatitis, we studied the activation of the classical and alternative pathways in patients with alcoholic hepatitis (n = 20), inactive alcoholic cirrhosis (n = 8), heavy drinkers without alcoholic liver disease (n = 10), patients with liver disease of nonalcoholic etiology (n = 11), and healthy control subjects (n = 18). Complement activation was evaluated in the alcoholic hepatitis patients by its correlation with a number of clinical and laboratory features indicative of the severity of liver injury, as well as by comparison of the patient groups. There was no significant difference in circulating C3 [1.02 g/liter, confidence interval (CI) = 0.76-1.28] or C4 (0.25 g/liter, CI = 0.17-0.33) in patients with alcoholic hepatitis when compared with the four control groups. Factor B levels (0.24 g/liter, CI = 0.21-0.27) were higher in the alcoholic hepatitis patients than the control groups (p < 0.01). However, activation of complement (given by the ratios C3d/C3, C4d/C4, and Ba/factor B) was not different in alcoholic hepatitis patients when compared with the control groups. Univariate analysis of a wide range of clinical and laboratory features in the alcoholic hepatitis subjects showed a positive correlation between plasma C3 and serum alkaline phosphatase (r = 0.68, p = 0.0014), AST (r = 0.55, p = 0.015), and gamma-glutamyltranspeptidase (r = 0.47, p = 0.035), but no correlation with clinical or laboratory features associated with high morbidity or mortality. There is no relationship between clinical or laboratory indicators of disease severity and complement activation, and it is unlikely that complement activation contributes to the clinical and histological features of alcoholic liver disease.
Alcoholic Hepatitis
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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.
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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
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Alcoholic Hepatitis
Steatohepatitis
Steatosis
Liver disease
Chronic liver disease
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Alcoholic Hepatitis
Alcohol abuse
Liver disease
Alcoholic fatty liver
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Alcoholic Hepatitis
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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
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