title: Enhanced cortisol suppression in response to dexamethasone administration in traumatized veterans with and without posttraumatic stress disorder.
abstract: BACKGROUND
  While enhanced cortisol suppression in response to dexamethasone is one of the most consistent biological findings in posttraumatic stress disorder (PTSD), the relative contribution of trauma exposure to this finding remains unclear.
  
  
  METHODS
  Assessment of diurnal salivary cortisol levels and 1600 h salivary cortisol before and after oral administration of 0.5mg dexamethasone in veterans with PTSD, veterans without PTSD (trauma controls) and healthy controls. Assessment of 1600 h plasma cortisol, ACTH and corticotrophin binding globulin (CBG) in response to dexamethasone in PTSD patients and trauma controls.
  
  
  RESULTS
  Both PTSD patients and trauma controls demonstrated significantly more salivary cortisol suppression compared to healthy controls. Salivary cortisol, plasma cortisol and ACTH suppression as well as CBG levels did not differ between PTSD patients and trauma controls. PTSD patients showed a reduced awakening cortisol response (ACR) compared to healthy controls that correlated significantly with PTSD symptoms. No significant differences were observed in ACR between PTSD patients and trauma controls.
  
  
  CONCLUSIONS
  These data suggest that enhanced cortisol suppression to dexamethasone is related to trauma exposure and not specifically to PTSD. The correlation between the ACR and PTSD severity suggests that a flattened ACR may be a result of clinical symptoms.
authors.affiliation: Department of Military Psychiatry, Central Military Hospital, Utrecht, The Netherlands. c.s.dekloet@umcutrecht.nl <c.s.dekloet@umcutrecht.nl>
authors.forename: C S
authors.initials: CS
authors.lastname: de Kloet
authors.forename: E
authors.initials: E
authors.lastname: Vermetten
authors.forename: C J
authors.initials: CJ
authors.lastname: Heijnen
authors.forename: E
authors.initials: E
authors.lastname: Geuze
authors.forename: E G W M
authors.initials: EG
authors.lastname: Lentjes
authors.forename: H G M
authors.initials: HG
authors.lastname: Westenberg
mesh_terms: D000222:Adaptation, Physiological; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000704:Analysis of Variance; D019540:Area Under Curve; D002352:Carrier Proteins / Q000378:metabolism; D016022:Case-Control Studies; D002940:Circadian Rhythm; D003345:Corticosterone; D003865:Major Depressive Disorder / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D008297:Male; D016555:Matched-Pair Analysis; D008875:Middle Aged; D008887:Military Medicine; D012016:Reference Values; D012463:Saliva / Q000378:metabolism; D018709:Statistics, Nonparametric; D013268:Stimulation, Chemical; D013313:Stress Disorders, Post-Traumatic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology; D014728:Veterans / Q000523:psychology*; D014947:Wounds and Injuries / Q000378:metabolism / Q000503:physiopathology
chemical_list: D002352:Carrier Proteins; D005938:Glucocorticoids; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone; D006854:Hydrocortisone