Determination of the source of androgen excess in functionally atypical polycystic ovary syndrome by a short dexamethasone androgen-suppression test and a low-dose ACTH test

Hum Reprod. 2011 Nov;26(11):3138-46. doi: 10.1093/humrep/der291. Epub 2011 Sep 9.


Background: Polycystic ovary syndrome (PCOS) patients typically have 17-hydroxyprogesterone (17OHP) hyperresponsiveness to GnRH agonist (GnRHa) (PCOS-T). The objective of this study was to determine the source of androgen excess in the one-third of PCOS patients who atypically lack this type of ovarian dysfunction (PCOS-A).

Methods: Aged-matched PCOS-T (n= 40), PCOS-A (n= 20) and controls (n= 39) were studied prospectively in a General Clinical Research Center. Short (4 h) and long (4-7 day) dexamethasone androgen-suppression tests (SDAST and LDAST, respectively) were compared in subsets of subjects. Responses to SDAST and low-dose adrenocorticotropic hormone (ACTH) were then evaluated in all.

Results: Testosterone post-SDAST correlated significantly with testosterone post-LDAST and 17OHP post-GnRHa (r = 0.671-0.672), indicating that all detect related aspects of ovarian dysfunction. An elevated dehydroepiandrosterone peak in response to ACTH, which defined functional adrenal hyperandrogenism, was similarly prevalent in PCOS-T (27.5%) and PCOS-A (30%) and correlated significantly with baseline dehydroepiandrosterone sulfate (DHEAS) (r = 0.708). Functional ovarian hyperandrogenism was detected by subnormal testosterone suppression by SDAST in most (92.5%) PCOS-T, but significantly fewer PCOS-A (60%, P< 0.01). Glucose intolerance was absent in PCOS-A, but present in 30% of PCOS-T (P < 0.001). Most of the PCOS-A cases with normal testosterone suppression in response to SDAST (5/8) lacked evidence of adrenal hyperandrogenism and were obese.

Conclusions: Functional ovarian hyperandrogenism was not demonstrable by SDAST in 40% of PCOS-A. Most of these cases had no evidence of adrenal hyperandrogenism. Obesity may account for most hyperandrogenemic anovulation that lacks a glandular source of excess androgen, and the SDAST seems useful in making this distinction.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • 17-alpha-Hydroxyprogesterone / metabolism
  • Adrenal Glands / metabolism
  • Adrenocorticotropic Hormone / blood*
  • Adult
  • Androgens / metabolism*
  • Body Mass Index
  • Dexamethasone / administration & dosage
  • Dexamethasone / pharmacology*
  • Female
  • Glucose Tolerance Test
  • Humans
  • Ovary / metabolism
  • Phenotype
  • Polycystic Ovary Syndrome / drug therapy*
  • Prospective Studies
  • Regression Analysis
  • Testosterone / pharmacology


  • Androgens
  • Testosterone
  • 17-alpha-Hydroxyprogesterone
  • Dexamethasone
  • Adrenocorticotropic Hormone