Abstract
Five patients with congenital adrenal hyperplasia due to an incomplete deficiency of 21-hydroxylation were treated by aminoglutethimide administered separately or in combination with dexamethasone. The results indicate that AG possesses an inhibitory action on 21- and 11-hydroxylations, more evident in patients with a preexisting incomplete defect of a hydroxylation than in normal subjects. AG may thus serve as a challenger, making obvious an incomplete enzymatic defect. The qualitatively different change of pregnantriol excretion in response to AG (increase) as compared to control subjects (decrease) may serve as a dynamic approach permitting the recognition of an incomplete subclinical defect of 21-hydroxylation.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
