help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pardini, D. P.
Right arrow Articles by Biglieri, E. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pardini, D. P.
Right arrow Articles by Biglieri, E. G.

Journal of Clinical Endocrinology & Metabolism, Vol 57, 1061-1066, Copyright © 1983 by Endocrine Society

ARTICLES

Impaired mineralocorticoid hormone responses to adrenocorticotropin stimulation: additional characterization of heterozygosity for the 21- hydroxylase deficiency type of congenital adrenal hyperplasia

DP Pardini, CE Kater, JG Vieira and EG Biglieri

In 12 obligate heterozygotes for the simple virilizing form of congenital adrenal hyperplasia (21-hydroxylase deficiency), basal and ACTH-stimulated levels of aldosterone, corticosterone, deoxycorticosterone, 18-hydroxycorticosterone, and 18- hydroxydeoxycorticosterone were examined. The responses to ACTH were significantly impaired (P less than 0.025 less than 0.001) compared with those of normal subjects. In addition to the often exaggerated stimulation by ACTH of the immediate precursor to 21-hydroxylation, 17 alpha-hydroxyprogesterone, the heterozygotes can now be characterized further by the impaired ACTH responses of mineralocorticoids distal to the block in the zona fasciculata; the ACTH-stimulated 17 alpha- hydroxyprogesterone/18-hydroxydeoxycorticosterone ratio was greater than normal in 94% of the heterozygotes. A limitation of 21- hydroxylation may also exist in the zona glomerulosa.


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
E. S. Knochenhauer, C. Cortet-Rudelli, R. D. Cunnigham, B. A. Conway-Myers, D. Dewailly, and R. Azziz
Carriers of 21-Hydroxylase Deficiency Are Not at Increased Risk for Hyperandrogenism
J. Clin. Endocrinol. Metab., February 1, 1997; 82(2): 479 - 485.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1983 by The Endocrine Society