title: Cortisol production rate in posttraumatic stress disorder.
abstract: BACKGROUND
  Several authors have reported the unsuspected finding of low cortisol levels (urinary, salivary, and serum) in patients with posttraumatic stress disorder (PTSD).
  
  
  OBJECTIVE
  Our objective was to assess concentrations of cortisol and its predominant metabolites, cortisol production rate (CPR), and glucocorticoid receptor (GR) binding characteristics in PTSD compared with normal subjects.
  
  
  METHODS
  Matched PTSD patients and control subjects had CPR determined by a stable isotope dilution technique after infusion of deuterated cortisol. Serum cortisol, urinary cortisol, and its metabolites were measured by gas chromatography/mass spectrometry. GR binding capacity (R(o)) and ligand binding affinity (K(d)) were measured in mononuclear leukocytes.
  
  
  METHODS
  All subjects were tested during a 40-h admission in an inpatient clinical research center.
  
  
  METHODS
  Ten patients with PTSD were matched by age and gender with 10 controls.
  
  
  METHODS
  Statistical comparison was conducted for various measures of cortisol in PTSD patients and normal subjects.
  
  
  RESULTS
  No statistical difference was found in mean level or circadian pattern of cortisol secretion using serum or salivary immunoassay detection methods. Although in the normal range, urinary cortisol by immunoassay showed statistically lower values over a 24-h period in PTSD patients compared with controls. This finding was not confirmed by gas chromatography/mass spectrometry determination of cortisol or its metabolites. CPR was not statistically different between these groups. GR also showed no alteration in R(o) or K(d) between the groups.
  
  
  CONCLUSIONS
  The data indicate that PTSD in the chronic and unprovoked state is not characterized by an acute biological stress response.
authors.affiliation: Department of Psychiatry, UHN-80, Oregon Health and Sciences University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239-3098, USA. whelert@ohsu.edu
authors.forename: G H Trevor
authors.initials: GH
authors.lastname: Wheler
authors.forename: David
authors.initials: D
authors.lastname: Brandon
authors.forename: Aaron
authors.initials: A
authors.lastname: Clemons
authors.forename: Crystal
authors.initials: C
authors.lastname: Riley
authors.forename: John
authors.initials: J
authors.lastname: Kendall
authors.forename: D Lynn
authors.initials: DL
authors.lastname: Loriaux
authors.forename: J David
authors.initials: JD
authors.lastname: Kinzie
mesh_terms: D000328:Adult; D002940:Circadian Rhythm / Q000502:physiology; D003907:Dexamethasone / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis* / Q000097:blood / Q000652:urine; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism*; D008297:Male; D008676:Metanephrine / Q000652:urine; D009647:Normetanephrine / Q000652:urine; D010913:Pituitary-Adrenal System / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D013313:Stress Disorders, Post-Traumatic / Q000378:metabolism* / Q000652:urine
chemical_list: D011965:Receptors, Glucocorticoid; D009647:Normetanephrine; D008676:Metanephrine; D003907:Dexamethasone; D006854:Hydrocortisone