Mineralocorticoid receptor function in posttraumatic stress disorder after pretreatment with metyrapone.
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Mineralocorticoid receptor function in posttraumatic stress disorder after pretreatment with metyrapone. / Otte, Christian; Muhtz, Christoph; Daneshkhah, Sima; Yassouridis, Alexander; Kiefer, Falk; Wiedemann, Klaus; Kellner, Michael.
in: BIOL PSYCHIAT, Jahrgang 60, Nr. 7, 7, 2006, S. 784-787.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Mineralocorticoid receptor function in posttraumatic stress disorder after pretreatment with metyrapone.
AU - Otte, Christian
AU - Muhtz, Christoph
AU - Daneshkhah, Sima
AU - Yassouridis, Alexander
AU - Kiefer, Falk
AU - Wiedemann, Klaus
AU - Kellner, Michael
PY - 2006
Y1 - 2006
N2 - BACKGROUND: Alterations of mineralocorticoid receptor (MR) mediated negative feedback inhibition of cortisol might contribute to abnormalities of hypothalamic-pituitary adrenal (HPA) activity in posttraumatic stress disorder (PTSD). METHODS: In a placebo-controlled study, we examined 11 subjects with PTSD and 11 healthy controls between 14:00 and 21:00. After pretreatment with 3 g metyrapone to inhibit basal endogenous cortisol secretion, subjects orally received in randomized order .5 mg of the MR agonist fludrocortisone or placebo. Adrenocorticotropic hormone (ACTH), cortisol, and 11-deoxycortisol were measured every 30 min until 21:00. RESULTS: Compared to placebo, fludrocortisone led to a significant decrease of ACTH and cortisol that was similar in both groups. Subjects with PTSD had higher raw cortisol and higher normed (baseline-related) ACTH and 11-deoxycortisol values after metyrapone independent of treatment with fludrocortisone or placebo. CONCLUSIONS: While HPA responses after metyrapone seem to be stronger in PTSD compared to controls, no alterations of mineralocorticoid receptor function in PTSD were found in this study.
AB - BACKGROUND: Alterations of mineralocorticoid receptor (MR) mediated negative feedback inhibition of cortisol might contribute to abnormalities of hypothalamic-pituitary adrenal (HPA) activity in posttraumatic stress disorder (PTSD). METHODS: In a placebo-controlled study, we examined 11 subjects with PTSD and 11 healthy controls between 14:00 and 21:00. After pretreatment with 3 g metyrapone to inhibit basal endogenous cortisol secretion, subjects orally received in randomized order .5 mg of the MR agonist fludrocortisone or placebo. Adrenocorticotropic hormone (ACTH), cortisol, and 11-deoxycortisol were measured every 30 min until 21:00. RESULTS: Compared to placebo, fludrocortisone led to a significant decrease of ACTH and cortisol that was similar in both groups. Subjects with PTSD had higher raw cortisol and higher normed (baseline-related) ACTH and 11-deoxycortisol values after metyrapone independent of treatment with fludrocortisone or placebo. CONCLUSIONS: While HPA responses after metyrapone seem to be stronger in PTSD compared to controls, no alterations of mineralocorticoid receptor function in PTSD were found in this study.
M3 - SCORING: Zeitschriftenaufsatz
VL - 60
SP - 784
EP - 787
JO - BIOL PSYCHIAT
JF - BIOL PSYCHIAT
SN - 0006-3223
IS - 7
M1 - 7
ER -