title: Adrenal glucocorticoid and androgen precursor dissociation in anorexia nervosa.
abstract: BACKGROUND
  Anorexia nervosa is characterized by hypogonadism and relative hypercortisolemia. We have demonstrated that free testosterone levels are low in women with anorexia nervosa, with the lowest levels in those receiving oral contraceptives (OCPs), and that dehydroepiandrosterone (DHEA) sulfate is reduced only in those receiving OCPs.
  
  
  OBJECTIVE
  The aim of the study was to determine whether adrenal steroidogenesis dysregulation contributes to decreased androgen levels in anorexia nervosa.
  
  
  METHODS
  We conducted a cross-sectional study in a General Clinical Research Center.
  
  
  METHODS
  We studied 20 women with anorexia nervosa [10 women with anorexia nervosa receiving OCPs (AN+E) and 10 not receiving OCPs (AN-E)] and 20 healthy controls [10 healthy controls receiving OCPs (HC+E) and 10 not receiving OCPs (HC-E)].
  
  
  METHODS
  We measured DHEA and cortisol levels in response to 250-microg cosyntropin stimulation after 1-mg overnight dexamethasone suppression.
  
  
  RESULTS
  Mean basal and stimulated, peak stimulated, and area under the curve (AUC) cortisol levels were higher in AN-E than HC-E, but mean basal and stimulated, peak and AUC DHEA were comparable. Mean AUC and peak cortisol were higher and DHEA AUC was lower in AN+E than AN-E. However, after controlling for cortisol binding globulin levels, peak and AUC cortisol were comparable between AN+E and AN-E. After controlling for albumin levels, AUC DHEA was comparable between AN+E and AN-E.
  
  
  CONCLUSIONS
  Adrenal glucocorticoid and androgen precursor secretion are dissociated in anorexia nervosa, with relative hypercortisolemia and a preservation of DHEA secretion. Reduced DHEA response to cosyntropin in women receiving OCPs is attributable to decreased albumin levels. In the setting of relative hypercortisolemia, reduced adrenal androgen precursor secretion is not a mechanism underlying low testosterone levels in anorexia nervosa.
authors.affiliation: Neuroendocrine Unit and General Clinical Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Lawson
authors.forename: M
authors.initials: M
authors.lastname: Misra
authors.forename: E
authors.initials: E
authors.lastname: Meenaghan
authors.forename: L
authors.initials: L
authors.lastname: Rosenblum
authors.forename: D A
authors.initials: DA
authors.lastname: Donoho
authors.forename: D
authors.initials: D
authors.lastname: Herzog
authors.forename: A
authors.initials: A
authors.lastname: Klibanski
authors.forename: K K
authors.initials: KK
authors.lastname: Miller
mesh_terms: D000328:Adult; D000856:Anorexia Nervosa / Q000097:blood*; D019540:Area Under Curve; D003276:Contraceptives, Oral / Q000494:pharmacology; D003430:Cross-Sectional Studies; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D012016:Reference Values; D013739:Testosterone / Q000097:blood
chemical_list: D003276:Contraceptives, Oral; D013739:Testosterone; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D006854:Hydrocortisone