Mineralocorticoid Receptor Function in Posttraumatic Stress Disorder After Pretreatment with Metyrapone

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• 作者：Christian Otte ; Christoph Muhtz ; Sima Daneshkhah ; Alexander Yassouridis ; Falk Kiefer ; Klaus Wiedemann and Michael Kellner
• 刊名：Biological Psychiatry
• 出版年：2006
• 出版时间：1 October 2006
• 年：2006
• 卷：60
• 期：7
• 页码：784-787
• 全文大小：197 K

文摘

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.