title: Increased androgen response to follicle-stimulating hormone administration in women with polycystic ovary syndrome.
abstract: BACKGROUND
  In women with polycystic ovary syndrome (PCOS), excess ovarian androgen production is driven by increased LH secretion. Studies conducted in animals suggest that the granulosa cell may influence LH-stimulated theca cell androgen production.
  
  
  OBJECTIVE
  The objective of this study was to determine whether FSH enhances androgen production in women with PCOS compared with that of normal women.
  
  
  METHODS
  A prospective study was conducted to compare androgen production in response to FSH in two groups of women.
  
  
  METHODS
  The study was conducted in a General Clinical Research Center in a tertiary academic medical center.
  
  
  METHODS
  Women with PCOS, 18-35 yr (n = 20), and normal ovulatory controls, 18-35 yr (n = 10), were recruited for study.
  
  
  METHODS
  Serial blood samples were obtained over a 24-h period after an iv injection of recombinant human FSH (150 IU).
  
  
  METHODS
  The main outcome measures were serum 17-hydroxyprogesterone (17-OHP), androstenedione (A), dehydroepiandrosterone (DHEA), testosterone (T), and inhibin B (Inh B) responses after FSH administration.
  
  
  RESULTS
  Basal serum 17-OHP, A, and T levels were markedly increased in women with PCOS compared with that observed in normal women. Basal DHEA and Inh B levels were similar to those of normal controls. After FSH injection, PCOS women demonstrated enhanced production of 17-OHP, A, DHEA, and Inh B, whereas in normal women no increases were observed. T levels declined slightly in both groups.
  
  
  CONCLUSIONS
  These findings provide evidence that, in PCOS women, theca cell androgen production is enhanced by FSH administration and suggest a granulosa-theca cell paracrine mechanism.
authors.affiliation: Department of Reproductive Medicine, School of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0633, USA.
authors.forename: Deborah S
authors.initials: DS
authors.lastname: Wachs
authors.forename: Mickey S
authors.initials: MS
authors.lastname: Coffler
authors.forename: Pamela J
authors.initials: PJ
authors.lastname: Malcom
authors.forename: Shunichi
authors.initials: S
authors.lastname: Shimasaki
authors.forename: R Jeffrey
authors.initials: RJ
authors.lastname: Chang
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000293:Adolescent; D000328:Adult; D000728:Androgens / Q000096:biosynthesis*; D000735:Androstenedione / Q000097:blood; D003687:Dehydroepiandrosterone / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007265:Inhibins / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D011446:Prospective Studies; D013739:Testosterone / Q000097:blood
chemical_list: D000728:Androgens; C422364:inhibin B; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D004958:Estradiol; D007265:Inhibins; D019326:17-alpha-Hydroxyprogesterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone