
Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.
Vitamin K, Ethanol, Pyridoxine, Anemia, Vitamin B 12 Deficiency, Lymphocyte Activation, Diet, Hepatitis, Alcoholism, Animals, Humans, Rabbits, Macrophage Migration-Inhibitory Factors
Vitamin K, Ethanol, Pyridoxine, Anemia, Vitamin B 12 Deficiency, Lymphocyte Activation, Diet, Hepatitis, Alcoholism, Animals, Humans, Rabbits, Macrophage Migration-Inhibitory Factors
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