title: Adrenocortical hyperresponsiveness to corticotropin in polycystic ovary syndrome patients with adrenal androgen excess.
abstract: OBJECTIVE
  To test the hypothesis that adrenal androgen (AA) excess in the polycystic ovary syndrome (PCOS) is due to a generalized exaggeration in AA output in response to adrenocorticotropic hormone (ACTH), and that this abnormality is due to an identifiable alteration in the biosynthesis of AAs.
  
  
  METHODS
  Cross-sectional prospective controlled study.
  
  
  METHODS
  Academic tertiary care medical center.
  
  
  METHODS
  Patients with PCOS (n = 9) and without (n = 9) AA excess and controls (n = 12) without hyperandrogenism, matched for age and body mass.
  
  
  METHODS
  Acute 60-minute ACTH test was performed on patients.
  
  
  METHODS
  Basal levels of dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), free T, and basal (Steroid(0)) and the 60-minute ACTH-stimulated levels (Steroid(60)) of pregnenolone (PREG), progesterone (P4), 17-hydroxypregnenolone (17-HPREG), 17-hydroxyprogesterone (17-HP), dehydroepiandrosterone (DHEA), and androstenedione (A4) were measured. Adrenocortical activities of 17-hydroxylase (17-OH), 17,20-lyase, and 3beta-hydroxysteroid dehydrogenase were estimated from product to precursor ratio, using Steroid(60) values.
  
  
  RESULTS
  Compared with PCOS patients without AA excess, PCOS patients with AA excess demonstrated significantly greater levels of DHEA(0) and A4(60). PCOS patients with AA excess had significantly higher activity of delta(5)17-OH, compared with PCOS patients without AA excess.
  
  
  CONCLUSIONS
  Adrenal androgen excess in PCOS is associated with a greater delta(5)17-OH activity in response to ACTH.
authors.affiliation: Department of Obstetrics and Gynecology, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
authors.forename: Carlos
authors.initials: C
authors.lastname: Moran
authors.forename: Rosario
authors.initials: R
authors.lastname: Reyna
authors.forename: Larry S
authors.initials: LS
authors.lastname: Boots
authors.forename: Ricardo
authors.initials: R
authors.lastname: Azziz
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D015096:3-Hydroxysteroid Dehydrogenases / Q000097:blood; D000302:Adrenal Cortex / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism* / Q000494:pharmacology; D000328:Adult; D000735:Androstenedione / Q000097:blood; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D011284:Pregnenolone / Q000097:blood; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies; D013254:Steroid 17-alpha-Hydroxylase / Q000097:blood; D013739:Testosterone / Q000097:blood
chemical_list: D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D011374:Progesterone; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D011284:Pregnenolone; D000324:Adrenocorticotropic Hormone; D015096:3-Hydroxysteroid Dehydrogenases; D013254:Steroid 17-alpha-Hydroxylase