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G Stutz

Publications and source records attributed to G Stutz.

6 recordsLinked to original sources
PubMed1981

Alcohol-induced decrease in uroporphyrinogen decarboxylase activity in rat liver and spleen.

Chronic alcohol consumption in rats leads to a decrease in uroporphyrinogen decarboxylase activity in liver and spleen, associated with a pathologic porphyrinuria. These findings show the toxic effect of alcohol in the biochemical pathogenesis of chronic hepatic porphyria. The results confirm experimentally the transition of symptomatic coproporphyrinuria to chronic hepatic porphyria as observed in man, and the progression of biochemical phases of chronic hepatic prophyria into the clinical phase, i.e., the development from latent to manifest stages under chronic alcohol ingestion.

Alcoholism↗
PubMed1978

[Clinical aspects of alcohol induced liver injury (author's transl)].

Chronic alcohol consumption results in early biochemical and ultrastructural alterations of the hepatocyte which in turn may lead to alcoholic fatty liver as well as alcoholic hepatitis and via the central hyaline sclerosis to fibrosis and cirrhosis of the liver. Already at the stage of the alcoholic fatty liver an isolated increase of serum gamma-glutamyltransferase activity can often be observed; it results from hepatic microsomal enzyme induction and may facilitate early recognition of alcoholic liver injury. To establish the diagnosis, however, a histological examination of the liver is necessary. The therapy of alcohol-induced liver injury is based upon an absolute alcohol abstinence since alcohol itself or one of its metabolites are hepatotoxic.

Albumins↗