title: Clinical evidence for predominance of delta-5 steroid production in women with polycystic ovary syndrome.
abstract: BACKGROUND
  In women with polycystic ovary syndrome (PCOS), the basis for ovarian androgen overproduction involves an overall increase of steroidogenesis, notably in the delta-4 pathway. However, in vitro studies have suggested that excessive androgen production occurs predominantly through the delta-5 pathway.
  
  
  OBJECTIVE
  This study was performed to assess androgen dose-responses after human chorionic gonadotropin (hCG) stimulation in PCOS and normal women.
  
  
  METHODS
  We conducted a prospective study to compare androgen production after iv hCG in PCOS and normal women.
  
  
  METHODS
  The study was conducted in a General Clinical Research Center in an academic medical center.
  
  
  METHODS
  Women with PCOS (age, 18-37 yr; n = 10) and normal ovulatory controls (age, 18-37 yr; n = 11) were recruited.
  
  
  METHODS
  For dose-response studies, blood samples were obtained before and at 0.5, 24, and 48 h after iv recombinant hCG (1, 10, 25, 100, and 250 μg). A subset of subjects underwent frequent blood sampling over 24 h after iv injection of 25 μg of recombinant hCG.
  
  
  METHODS
  We measured basal and stimulated serum 17-hydroxyprogesterone (17-OHP), androstenedione (A), testosterone (T), dehydroepiandrosterone, estradiol, and progesterone responses after hCG administration.
  
  
  RESULTS
  In PCOS women, maximal A and T production was observed at the lowest doses of hCG, whereas responses were minimal in normal women. Incremental responses of 17-OHP, estradiol, and progesterone were greater in PCOS compared to normal women.
  
  
  CONCLUSIONS
  In PCOS women, maximal A and T responses to hCG relative to those of 17-OHP are consistent with ovarian androgen overproduction via the delta-5 pathway.
authors.affiliation: Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093, USA.
authors.forename: Marcus A
authors.initials: MA
authors.lastname: Rosencrantz
authors.forename: Mickey S
authors.initials: MS
authors.lastname: Coffler
authors.forename: Annette
authors.initials: A
authors.lastname: Haggan
authors.forename: Kimberly B
authors.initials: KB
authors.lastname: Duke
authors.forename: Michael C
authors.initials: MC
authors.lastname: Donohue
authors.forename: Rana F
authors.initials: RF
authors.lastname: Shayya
authors.forename: H Irene
authors.initials: HI
authors.lastname: Su
authors.forename: R Jeffrey
authors.initials: RJ
authors.lastname: Chang
mesh_terms: D000293:Adolescent; D000328:Adult; D015992:Body Mass Index; D006063:Chorionic Gonadotropin / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D003687:Dehydroepiandrosterone / Q000097:blood / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood / Q000150:complications / Q000378:metabolism; D007275:Injections, Intravenous; D009839:Oligomenorrhea / Q000097:blood / Q000150:complications / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000378:metabolism*; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology; D013256:Steroids / Q000097:blood / Q000378:metabolism*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D006063:Chorionic Gonadotropin; D011994:Recombinant Proteins; D013256:Steroids; D003687:Dehydroepiandrosterone; D004958:Estradiol