Alcoholic hepatitis represents the most severe form of alcoholic liver disease Recent research points to an exaggerated inflammatory response, mediated by neutrophils,as the basic mechanism of liver damage. This entity has a distinctive clinical picture and a characteristic histopathology and a poor outcome.Recent investigation reveals a complex network of intracellular and intercellular communication signals involving hepatocytes, endothelial cells, monocytes, lymphocytes, neutrophils,Ito and Kupffer cells, leading to massive migration of neutrophils from blood to liver.When neutrophils reach the liver, multiple cytokines produced locally by endothelium, hepatocytes and Kupffer cells, up-regulate their function. Activation of neutrophils leads to increased production of oxygen radicals(mainly superoxide)and hydrogen peroxide production.To date there is general agreement that measurement of superoxide production by neutrophils is a reliable way of determining neutrophil function and its activation.Thirty one patients with acute alcoholic hepatitis, twenty with compensated alcoholic liver disease end seventeen controls were studied.Patients with alcoholic hepatitis and alcoholic liver disease were enrolled on admission to the hospital and if they had no features of infection, bleeding or renal failure.The neutrophil stimuli used were opsonized zymosan and fMLP.The production of superoxide was similar in the three groups when neutrophils were not stimulated.After stimulation with opsonized zymosan,there was an increase in the production of superoxide from patients with acute alcoholic hepatitis in comparison to those with alcoholic liver disease and controls. This increase was statistically significant when fMLP was the stimulant(p<0.05). This is a reliable technique that can be use in the evaluation of different therapeutic modalities in acute alcoholic hepatitis
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