| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Clinical Endocrinology & Metabolism, Vol 55, 768-773, Copyright © 1982 by Endocrine Society
ARTICLES |
GC Lachelin, HL Judd, SC Swanson, ME Hauck, DC Parker and SS Yen
The long term effects of nightly dexamethasone administration on basal levels and diurnal fluctuations of circulating gonadotropins, androgens, and cortisol were studied by frequent sampling in four women with polycystic ovarian disease and a similar number of normal women. Basal LH, testosterone, and androstenedione levels were elevated in the patients with polycystic ovarian disease. There were significant diurnal variations of all steroids measured in both groups, with the exception of androstenedione and androstenediol in the polycystic ovarian disease and control subjects, respectively. Nightly dexamethasone administration for 1 month resulted in marked suppression of dehydroepiandrosterone, androstenediol, and cortisol. For testosterone the mean percent decreases of the 24-h transverse means were 15% and 46% for the polycystic ovarian disease and normal subjects, respectively. For androstenedione the mean percent decreases were only 7% and 20%, respectively. The diurnal variation of all steroids disappeared with dexamethasone. These results support the concept that in patients with polycystic ovarian disease the majority of delta 5-androgens is adrenal while the preponderance of elevated testosterone and androstenedione is ovarian in origin. These results do not support the use of long term dexamethasone as an effective agent in suppressing the elevated levels of testosterone and androstenedione in patients with this disease.
This article has been cited by other articles:
![]() |
M. K. Tee, Q. Dong, and W. L. Miller Pathways Leading to Phosphorylation of P450c17 and to the Posttranslational Regulation of Androgen Biosynthesis Endocrinology, May 1, 2008; 149(5): 2667 - 2677. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Samandari, P. Kempna, J.-M. Nuoffer, G. Hofer, P. E Mullis, and C. E Fluck Human adrenal corticocarcinoma NCI-H295R cells produce more androgens than NCI-H295A cells and differ in 3{beta}-hydroxysteroid dehydrogenase type 2 and 17,20 lyase activities J. Endocrinol., December 1, 2007; 195(3): 459 - 472. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Kempna, G. Hofer, P. E. Mullis, and C. E. Fluck Pioglitazone Inhibits Androgen Production in NCI-H295R Cells by Regulating Gene Expression of CYP17 and HSD3B2 Mol. Pharmacol., March 1, 2007; 71(3): 787 - 798. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Fassnacht, N. Schlenz, S. B. Schneider, S. A. Wudy, B. Allolio, and W. Arlt Beyond Adrenal and Ovarian Androgen Generation: Increased Peripheral 5{alpha}-Reductase Activity in Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2760 - 2766. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. W. M. Martens, D. H. Geller, W. Arlt, R. J. Auchus, V. S. Ossovskaya, H. Rodriguez, A. Dunaif, and W. L. Miller Enzymatic Activities of P450c17 Stably Expressed in Fibroblasts from Patients with the Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., November 1, 2000; 85(11): 4338 - 4346. [Abstract] [Full Text] |
||||
![]() |
R. Azziz, V. Y. Black, E. S. Knochenhauer, G. A. Hines, and L. R. Boots Ovulation After Glucocorticoid Suppression of Adrenal Androgens in the Polycystic Ovary Syndrome Is Not Predicted by the Basal Dehydroepiandrosterone Sulfate Level J. Clin. Endocrinol. Metab., March 1, 1999; 84(3): 946 - 950. [Abstract] [Full Text] |
||||
| 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 |