Alcohol is the most significant liver poison. Its degradation takes above all place by the alcohol dehydrogenase and the microsomal alcohol-oxidizing system. In the first step of degradation acetaldehyde develops which in enrichment evokes immediately toxic defects on the mitochondrias of the cells of the liver parenchyma and thus introduces a vicious circle. Furthermore, an increased affection of pharmacometabolites as a sequel of the alcohol-conditioned enzyme induction may lead to a defect. Alcohol influences intermediary metabolic functions: the gluconeogenesis is inhibited, multi-layer disturbances in the lipid metabolism lead to fatty degeneration of the liver. A hyperuricaemia results from overproduction in the liver as well as from decreased renal excretion. The proline formation is increased. Distinct increase of the gamma-GT-activity is an early and relatively specific indicator of the alcoholic liver defect. Morphologic and clinical manifestations are fatty degeneration of the liver, hepatitis based on fatty degeneration of the liver and cirrhosis. Apart from dose and duration of the alcohol intake additional factors require consideration. The author adopts a definite attitude to etiopathogeneis and therapeutic possibilities.
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