Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome

F. Gonzalez, L. Chang, T. Horab, R. A. Lobo

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Objective: To examine the hypothesis that, in polycystic ovary syndrome (PCOS), ovarian steroids induce adrenal enzyme dysfunction or adrenal androgen hyperresponsiveness to ACTH. Design: Prospective controlled clinical study. Setting: Reproductive endocrinology unit of an academic medical center. Patients: Twelve women with PCOS who had adrenal androgen excess were compared with five weight-matched ovulatory women. In half of the women with PCOS, prestudy screening was suggestive of mild 3β-hydroxysteroid dehydrogenase (HSD) deficiency. Interventions: Basal and adrenal dynamic blood sampling before and after GnRH agonist (GnRH-a) administration for 6 months. Main Outcome Measures: Basal E2 and androgen levels as well as dexamethasone-suppressed, ACTH-stimulated 17α-hydroxyprogesterone, 17α- hydroxypregnenolone, and androgen levels before and after ovarian suppression. Results: Although none of the subjects with PCOS proved to have mild 3β-HSD deficiency, the majority of them (58%) met the criteria for 17,20 lyase hyperactivity before and after GnRH-a therapy. As a group, the remaining subjects with PCOS exhibited an elevated DHEAS response to ACTH before GnRH-a treatment, which may have normalized after GnRH-a treatment. Conclusion: Adrenal androgen excess in PCOS may be heterogeneous in etiology, whereas 17,20 lyase hyperactivity appears to be an intrinsic adrenal disorder, adrenal androgen hyperresponsiveness to ACTH may be ovarian induced. Reliance on historical controls may lead to overdiagnosis of mild 3β-HSD deficiency.

Original languageEnglish (US)
Pages (from-to)354-361
Number of pages8
JournalFertility and Sterility
Volume66
Issue number3
StatePublished - 1996
Externally publishedYes

Fingerprint

Polycystic Ovary Syndrome
Androgens
3-Hydroxysteroid Dehydrogenases
Gonadotropin-Releasing Hormone
Adrenocorticotropic Hormone
Steroid 17-alpha-Hydroxylase
17-alpha-Hydroxypregnenolone
17-alpha-Hydroxyprogesterone
Endocrinology
Dexamethasone
Therapeutics
Steroids
Outcome Assessment (Health Care)
Weights and Measures
Enzymes

Keywords

  • 17,20 lyase hyperactivity
  • adrenal androgen hyperresponsiveness to ACTH
  • adrenal dynamic testing
  • GnRH agonist
  • Polycystic ovary syndrome

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Gonzalez, F., Chang, L., Horab, T., & Lobo, R. A. (1996). Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome. Fertility and Sterility, 66(3), 354-361.

Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome. / Gonzalez, F.; Chang, L.; Horab, T.; Lobo, R. A.

In: Fertility and Sterility, Vol. 66, No. 3, 1996, p. 354-361.

Research output: Contribution to journalArticle

Gonzalez, F, Chang, L, Horab, T & Lobo, RA 1996, 'Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome', Fertility and Sterility, vol. 66, no. 3, pp. 354-361.
Gonzalez, F. ; Chang, L. ; Horab, T. ; Lobo, R. A. / Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome. In: Fertility and Sterility. 1996 ; Vol. 66, No. 3. pp. 354-361.
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