title: 11 beta-hydroxyandrostenedione in plasma, follicular fluid, and granulosa cells of women with normal and polycystic ovaries.
abstract: OBJECTIVE
  To investigate the role of 11 beta-hydroxylase/11 beta-hydroxyandrostenedione (11-OHA) in the ovarian metabolism of androgens in women with polycystic ovaries (PCO) and its associated syndrome (PCOS).
  
  
  METHODS
  Prospective observational study examining the plasma and follicular fluid (FF) concentrations of 11-OHA, testosterone (T), androstenedione (A), and cortisol from women with PCOS and normal women in spontaneous and stimulated cycles.
  
  
  METHODS
  The study was carried out in an infertility department and an endocrine research laboratory of a university hospital.
  
  
  METHODS
  Five groups of women were studied. Blood was taken from 53 women with PCOS and 13 normal controls. Follicular fluid and blood was obtained from 51 women with stimulated cycles undergoing in vitro fertilization embryo-transfer (IVF-ET), 27 of whom had PCO and 24 had normal ovaries. Follicular fluid alone was also taken from 13 women with normal ovaries undergoing laparoscopies.
  
  
  METHODS
  Clear FF was obtained for analysis during oocyte collection. Granulosa cells (GCs) were obtained from seven women with PCO undergoing IVF-ET and were incubated with radiolabeled substrates.
  
  
  RESULTS
  Circulating concentrations of T and 11-OHA were higher in women with PCOS compared with women with normal ovaries. In women with PCO receiving exogenous gonadotropin, only 11-OHA concentrations were higher. Concentrations of all steroids measured were higher in FF than plasma, with plasma 11-OHA concentrations 4 to 12 times higher in FF. Significantly lower concentrations of 11-OHA were found in the FF of women with PCO compared with women with normal ovaries. There was no evidence of 11 beta-hydroxylation of A by GCs.
  
  
  CONCLUSIONS
  Although the raised plasma concentrations of 11-OHA may reflect hyperandrogenism in PCOS and lower 11-OHA concentrations in FF in women with PCO suggest abnormal androgen metabolism, neither can be regarded as a marker for this syndrome.
authors.affiliation: Cobbold Laboratories, University College and Middlesex Hospital School of Medicine, London, United Kingdom.
authors.forename: E J
authors.initials: EJ
authors.lastname: Owen
authors.forename: P
authors.initials: P
authors.lastname: Holownia
authors.forename: G S
authors.initials: GS
authors.lastname: Conway
authors.forename: H S
authors.initials: HS
authors.lastname: Jacobs
authors.forename: J W
authors.initials: JW
authors.lastname: Honour
mesh_terms: D000735:Androstenedione / Q000031:analogs & derivatives* / Q000032:analysis / Q000097:blood; D002478:Cells, Cultured; D005260:Female; D015571:Follicular Fluid / Q000737:chemistry*; D006107:Granulosa Cells / Q000737:chemistry*; D006801:Humans; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*; D011446:Prospective Studies; D013739:Testosterone / Q000097:blood
chemical_list: D013739:Testosterone; D000735:Androstenedione; C003582:11-hydroxyandrostenedione