| pubmed-article:359965 | pubmed:abstractText | Alcohol is a agenrphyrinogenic agent which may cause disturbances in porphyrin metabolism in healthy persons as well as biochemical and clinical manifestations of acute and chronic hepatic porphyrias. After excessive alcohol infestion in man a secondary hepatic coproporphyrinuria develops transiently, which persists in alcoholic liver disease. The alcohol-liver-porphyrinuria syndrome ranges first among the secondary hepatic disturbances of porphyrin metabolism. In acute hepatic porphyrias (acute intermittent porphyria, porphyria varigata and hereditary coproporphyria) alcohol induces delta-aminolevulinic acid synthase because in these porphyrias the control mechanisms of porphyrinogen and heme synthesis in liver are disturbed ("molecular regulatory diseases"). On the contrary, in chronic hepatic porphyrias, which are already associated with liver damage ("membrane diseases"), alcohol potentiates the disturbance of the decarboxylation of uro- and heptacarboxyporphyrinogen, which is followed by a hepatic accumulation of uro- and heptacarboxyporphyrin and their sometimes extreme urinary excretion. Alcohol may transform a symptomatic coproporphyrinuria into chronic hepatic porphyria. One can deduct from experimental and clinical studies that in liver alcohol inhibits the enzymes coproporphyrinogen oxidase, delta-aminolevulinic acid dehydratase and uroporphyrinogen decarboxylase and induces delta-aminolevulinic acid synthase. Abstinence from alcohol is an important measure in the therapy and prophylaxis of all hepatic porphyrias. | lld:pubmed |
