English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Blunted ACTH response to dexamethasone suppression-CRH stimulation in posttraumatic stress disorder

MPS-Authors
/persons/resource/persons80445

Modell,  S.
Max Planck Institute of Psychiatry, Max Planck Society;

/persons/resource/persons80372

Holsboer,  F.
Florian Holsboer (Direktor), Max Planck Institute of Psychiatry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Ströhle, A., Scheel, M., Modell, S., & Holsboer, F. (2008). Blunted ACTH response to dexamethasone suppression-CRH stimulation in posttraumatic stress disorder. Journal of Psychiatric Research, 42(14), 1185-1188.


Cite as: https://hdl.handle.net/11858/00-001M-0000-000E-93C3-8
Abstract
Previous studies have suggested that patients with posttraumatic stress disorder (PTSD) have an enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) system and a blunted ACTH response to corticotropin releasing hormone (CRH). The effects of two dexamethasone dosages (0.75 and 1.5 mg) on the ACTH and cortisol concentrations after CRH stimulation (100 mu g) were studied in eight patients with PTSD and matched healthy control subjects. Compared to healthy subjects, patients with PTSD have a blunted ACTH response to CRH. Cortisol concentrations were only significantly influenced by dexamethasone dosage. Our results give further evidence for a central role of the pituitary in reflecting changes of the negative feedback sensitivity of the HPA system in patients with PTSD. (C) 2008 Elsevier Ltd. All rights reserved.