THE CONCOMITANT RELEASE OF ANDROSTENEDIONE WITH CORTISOL AND LUTEINIZING-HORMONE PULSATILE RELEASES DISTINGUISHES ADRENAL FROM OVARIAN HYPERANDROGENISM

Citation
Ad. Genazzani et al., THE CONCOMITANT RELEASE OF ANDROSTENEDIONE WITH CORTISOL AND LUTEINIZING-HORMONE PULSATILE RELEASES DISTINGUISHES ADRENAL FROM OVARIAN HYPERANDROGENISM, Gynecological endocrinology, 7(1), 1993, pp. 33-41
Citations number
NO
Categorie Soggetti
Endocrynology & Metabolism","Obsetric & Gynecology
Journal title
ISSN journal
09513590
Volume
7
Issue
1
Year of publication
1993
Pages
33 - 41
Database
ISI
SICI code
0951-3590(1993)7:1<33:TCROAW>2.0.ZU;2-3
Abstract
Androstenedione secretory characteristics and its possible temporal co rrelation with luteinizing hormone (LH) and/or cortisol, intended as t he markers of, respectively, ovarian stimulation and adrenal secretion , were evaluated in 24 patients affected by dinical hyperandrogenism. A pulsatility test was carried out for 8 h, with sampling every 10 min , and LH, cortisol and androstenedione profiles were determined by rad ioimmunoassay. Time series were analyzed with the computer program DET ECT and with a program for specific concordance estimation. A distinct episodic release of LH, cortisol and androstenedione was observed in all patients (6.9 +/- 0.8, 5.2 +/- 0.6 and 5.5 +/- 1 peaks/8 h, respec tively). When specific concordance was tested between LH and androsten edione, and between cortisol and androstenedione, two distinct groups of patients could be identified. Group A (n = 13) showed a significant specific concordance (SC) index only for LH and androstenedione whik group B (n = 11) showed a significant SC also for cortisol and androst enedione, thus demonstrating a consistent adrenal participation in the androstenedione secretion in these patients. In addition, specific di fferences were observed on androstenedione secretory profiles of group B which showed a significant (p < 0.05) decrease of androstenedione p lasma concentrations emulating cortisol behavior. No such observation was noted in group A, whose androstenedione plasma levels did not show any reduction. In conclusion, our data support the use of circulating androstenedione, LH and cortisol plasma levels and copulsatile assess ment to distinguish the presence of two populations of hyperandrogenic patients: one whose hyperandrostenedionemia is mainly due to ovarian secretion (group A) and one which showed a hyperactivation of the adre nal gland (group B). This observation can be helpful for ensuring a co rrect therapeutical approach to the hyperandrogenic patient.