title: Lack of Serum anti-Mullerian hormone responses after recombinant human chorionic gonadotropin stimulation in women with polycystic ovary syndrome.
abstract: BACKGROUND
  Polycystic ovary syndrome (PCOS) is an anovulatory disorder characterized by excess androgen production and increased LH secretion. Serum anti-Mullerian hormone (AMH) is also elevated in this disorder. Women with PCOS exhibit a positive correlation between AMH and LH levels and recent in vitro data demonstrate that LH can directly stimulate AMH production by granulosa cells from women with PCOS.
  
  
  OBJECTIVE
  The objective of the study was to directly test whether LH increases AMH production in women with PCOS in vivo by assessing responses after recombinant human chorionic gonadotropin (r-hCG) stimulation.
  
  
  METHODS
  This was a prospective study.
  
  
  METHODS
  The study was conducted at a research center at an academic medical center.
  
  
  METHODS
  Women with PCOS (n = 28) and normal controls (n = 29) participated in the study.
  
  
  METHODS
  Blood samples were obtained before and 24 hours after iv administration of 25 μg r-hCG.
  
  
  METHODS
  Basal and stimulated serum AMH, androstenedione, T, and 17-hydroxyprogesterone levels were measured.
  
  
  RESULTS
  Baseline AMH levels in women with PCOS were greater than in normal controls and correlated with levels of LH as well as androstenedione, T, and 17-hydroxyprogesterone. A rise of serum AMH levels was not observed after r-hCG administration in women with PCOS or normal ovaries.
  
  
  CONCLUSIONS
  These findings are in contrast to in vitro evidence demonstrating that AMH secretion by granulosa cells of PCOS women in response to LH stimulation and suggest AMH regulation in vivo is complex and that the elevated serum AMH in women with PCOS is not a direct effect of the excess LH production characteristic of PCOS.
authors.affiliation: Department of Reproductive Medicine (H.C.-A., S.S.C., K.M., M.A.R., H.I.S., M.L., R.J.C.), University of California, San Diego, La Jolla California 92093; and Department of Clinical Development Sciences and Basic Medical Sciences (H.D.M.), St George's University of London, London SW17 ORE, United Kingdom.
authors.forename: Heidi
authors.initials: H
authors.lastname: Cook-Andersen
authors.forename: Sandy S
authors.initials: SS
authors.lastname: Chuan
authors.forename: Kevin
authors.initials: K
authors.lastname: Maas
authors.forename: Marcus A
authors.initials: MA
authors.lastname: Rosencrantz
authors.forename: H Irene
authors.initials: HI
authors.lastname: Su
authors.forename: Mark
authors.initials: M
authors.lastname: Lawson
authors.forename: Helen D
authors.initials: HD
authors.lastname: Mason
authors.forename: R Jeffrey
authors.initials: RJ
authors.lastname: Chang
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000328:Adult; D000735:Androstenedione / Q000097:blood; D054304:Anti-Mullerian Hormone / Q000097:blood*; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D005260:Female; D006801:Humans; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D011446:Prospective Studies; D013739:Testosterone / Q000097:blood
chemical_list: D006063:Chorionic Gonadotropin; D013739:Testosterone; D000735:Androstenedione; D019326:17-alpha-Hydroxyprogesterone; D054304:Anti-Mullerian Hormone