title: 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.
abstract: 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.
authors: Department of Pediatrics and Medicine, The University of Chicago Pritzker School of Medicine, Chicago, IL 60637, USA. robros@peds.bsd.uchicago.edu
authors: Robert L
authors: RL
authors: Rosenfield
authors: Monica
authors: M
authors: Mortensen
authors: Kristen
authors: K
authors: Wroblewski
authors: Elizabeth
authors: E
authors: Littlejohn
authors: David A
authors: DA
authors: Ehrmann
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000378:metabolism; D000311:Adrenal Glands / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000328:Adult; D000728:Androgens / Q000378:metabolism*; D015992:Body Mass Index; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D010053:Ovary / Q000378:metabolism; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy*; D011446:Prospective Studies; D012044:Regression Analysis; D013739:Testosterone / Q000494:pharmacology
chemical_list: D000728:Androgens; D013739:Testosterone; D019326:17-alpha-Hydroxyprogesterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone