Alcohol has an porphyrinogenic action and can cause a disturbance of porphyrin metabolism in healthy people as well as lead to a biochemical and clinical manifestation of acute and chronic hepatic porphyrias, especially acute intermittent porphyria and porphyria cutanea tarda. After excessive consumption of alcohol a temporary, clinically asymptomatic secondary hepatic coproporphyrinuria in man can be observed, which can become persistent in cases of alcohol-induced liver damage. Nowadays alcohol-liver-porphyrinuria syndrome is the first to be mentioned in secondary hepatic disturbances of porphyrin metabolism. In people with a genetic lack of uroporphyrinogen-decarboxylase alcohol is able to transform an asymptomatic coproporphyrinuria into a chronic hepatic porphyria or porphyria cutanea tarda. From experimental and clinical studies the conclusion can be drawn that alcohol inhibits the enzymes delta-aminolevulinic-acid-dehydratase (synonym: porphobilinogen-synthase), uroporphyrinogen-decarboxylase and coproporphyrinogen-oxidase and induces delta-aminolevulinic-acid-synthase in the liver. Abstinence of alcohol is a therapeutically and prophylactically important measurement in all types of hepatic porphyrias. For clinical experience follows that in cases with chronic consumption of alcohol, fatty liver, alcohol induced hepatitis and liver cirrhosis porphyrin studies in urine should be made to notice a hepatic porphyria in the latent phase very early. When dealing with abdominal and cutaneous symptoms in clinical context with consumption of alcohol one has to exclude hepatic porphyria differential diagnostically.