title: Role of the ovary in the adrenal androgen excess of hyperandrogenic women.
abstract: OBJECTIVE
  To test the hypothesis that ovarian hormones in women with hyperandrogenism alter adrenocortical steroidogenesis.
  
  
  METHODS
  Combination of two prospective studies.
  
  
  METHODS
  Academic medical centers.
  
  
  METHODS
  Eighteen hyperandrogenic patients demonstrating hirsutism with either hyperandrogenemia, oligomenorrhea, or both. Eighteen healthy nonhirsute eumenorrheic untreated women served as controls.
  
  
  METHODS
  Blood sampling basally and after acute adrenal stimulation with ACTH, before and after 20-24 weeks of leuprolide administration. Nine patients also received 0.625 mg/d of oral conjugated esterified estrogens and 10 mg of medroxyprogesterone acetate days 1-12 of the month (i.e., estrogen replacement therapy [ERT]), whereas the remaining nine did not.
  
  
  METHODS
  Before and after the administration of the GnRH agonist (GnRH-a), the basal concentrations of DHEAS; and the levels of androstenedione (A4), DHEA, androstenediol, 11 beta-hydroxyandrostenedione (11-OHA4), and cortisol before and 60 minutes after acute adrenal stimulation, were measured.
  
  
  RESULTS
  Levels of DHEAS, androstenediol, and 11-OHA4 decreased by 15%-30%, regardless of whether patients initially had or did not have DHEAS excess. However, only hyperandrogenic patients with elevated levels of DHEAS showed a significant decrease in basal DHEA levels. No statistically significant difference in the response of either androgen to ACTH (1-24) stimulation was noted with ovarian suppression, regardless of initial DHEAS level or use of ERT.
  
  
  CONCLUSIONS
  We found no evidence that ovarian hormone secretion affected adrenal steroidogenesis, and those women with the highest adrenal androgen levels had the least response to GnRH-a suppression. These findings further support the concept of an intrinsic, and possibly primary, abnormality of adrenocortical steroidogenesis in a subset of hyperandrogenic women that is independent of ovarian abnormalities.
authors.affiliation: The University of Alabama, Birmingham 35233-7333, USA. razziz@uabmc.edu
authors.forename: R
authors.initials: R
authors.lastname: Azziz
authors.forename: R S
authors.initials: RS
authors.lastname: Rittmaster
authors.forename: L M
authors.initials: LM
authors.lastname: Fox
authors.forename: E L
authors.initials: EL
authors.lastname: Bradley
authors.forename: H D
authors.initials: HD
authors.lastname: Potter
authors.forename: L R
authors.initials: LR
authors.lastname: Boots
mesh_terms: D000293:Adolescent; D000305:Adrenal Cortex Hormones / Q000096:biosynthesis*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000328:Adult; D000728:Androgens / Q000096:biosynthesis*; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D015914:Estrogen Replacement Therapy; D005260:Female; D006628:Hirsutism / Q000378:metabolism*; D006801:Humans; D016729:Leuprolide / Q000627:therapeutic use; D010053:Ovary / Q000378:metabolism*; D011446:Prospective Studies
chemical_list: D000305:Adrenal Cortex Hormones; D000728:Androgens; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D016729:Leuprolide