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Journal of Clinical Endocrinology & Metabolism, Vol 52, 549-552, Copyright © 1981 by Endocrine Society
ARTICLES |
MJ Hughes and AB Rifkind
Danazol (a derivative of 17 alpha-ethinyl testosterone) has recently been reported to cause clinical exacerbations of acute intermittent porphyria. In the present study, we demonstrate that danazol is an inducer of hepatic delta-aminolevulinic acid synthetase and that it increases hepatocyte porphyrin production using a chick embryo model. The findings provide an explanation for the clinical observations. Although danazol is a porphyrinogenic agent in the chick embryo and humans it has been reported to be ineffective as a porphyrinogen in rats. The present findings, therefore, also confirm the superiority of the chick embryo as a model system for the screening of drugs and chemicals which may have the potential to cause clinical exacerbations of porphyria.
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