help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
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 Zadik, Z.
Right arrow Articles by Hochberg, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zadik, Z.
Right arrow Articles by Hochberg, Z.

Journal of Clinical Endocrinology & Metabolism, Vol 58, 384-387, Copyright © 1984 by Endocrine Society

ARTICLES

Salt loss in hypertensive form of congenital adrenal hyperplasia (11- beta-hydroxylase deficiency)

Z Zadik, L Kahana, H Kaufman, A Benderli and Z Hochberg

Studies in patients with congenital adrenal hyperplasia due to 11- hydroxylase deficiency (11-OHD) suggest a common defect in the adrenal zona fasciculate and zona glomerulosa. The hypertension in untreated 11- OHD patients is considered to be secondary to the accumulation of deoxycorticosterone as a consequence of inadequate 11-beta- hydroxylation in the biosynthesis of aldosterone, and is alleviated by glucocorticoid suppression. To investigate whether deoxycorticosterone suppression in these patients resulted in loss of salt, 11 patients with 11-OHD aged 4-26 yr were studied. Patients were evaluated during dexamethasone suppression (0.6 mg/m for 2 weeks) while receiving a normal diet and a low salt diet (10 meq Na/24 h). There was no significant change in serum electrolytes, cortisol, 11-deoxycortisol, and DOC during these two dietary regimens. PRA in the recumbent and upright positions on both diets was significantly higher in the patients than in normal subjects. Plasma or urinary aldosterone levels were significantly lower in the 11-OHD patients than in the normal controls. Moderate salt loss occurred during the low salt diet. It is concluded that sodium retention is incomplete in glucocorticoid-treated 11-OHD patients. Partial sodium retention is maintained by increased PRA and a subnormal aldosterone response. 11-OHD patients should be carefully monitored during acute disease states and, when electrolyte imbalance is suspected, treatment with mineralocorticoid should be considered.


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
T. Paperna, R. Gershoni-Baruch, K. Badarneh, L. Kasinetz, and Z. Hochberg
Mutations in CYP11B1 and Congenital Adrenal Hyperplasia in Moroccan Jews
J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5463 - 5465.
[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 © 1984 by The Endocrine Society