The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder

@article{Yehuda2002TheCA,
  title={The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder},
  author={Rachel Yehuda and Sarah L. Halligan and Robert A Grossman and Julia A. Golier and Cheryl M. Wong},
  journal={Biological Psychiatry},
  year={2002},
  volume={52},
  pages={393-403}
}

Leukocyte glucocorticoid receptor expression and immunoregulation in veterans with and without post-traumatic stress disorder

TLDR
The results suggest that trauma exposure is sufficient to induce changes in GR binding characteristics, whereas resistance of T-cell proliferation to DEX only occurs in PTSD.

Alterations in Stress Reactivity After Long‐Term Treatment with Paroxetine in Women with Posttraumatic Stress Disorder

TLDR
Assessment of the effect of long‐term treatment with the selective reuptake inhibitor (SSRI), paroxetine, on stress reactivity in patients with PTSD suggests that successful treatment with SSRI in chronic PTSD is associated with a trend for a decrease in baseline diurnal cortisol and with reduced cortisol reactivity to stress.

The ACTH response to dexamethasone in PTSD.

TLDR
The data support the hypothesis of enhanced cortisol negative feedback inhibition of ACTH secretion at the level of the pituitary in PTSD, which is implicated as a likely mechanism for this effect.

Cortisol and post-traumatic stress disorder in adults

TLDR
Comparison of basal cortisol levels in adults with current PTSD and in people without psychiatric disorder revealed that studies assessing plasma or serum showed significantly lower levels in people with PTSD than in controls not exposed to trauma.

Maternal PTSD associates with greater glucocorticoid sensitivity in offspring of Holocaust survivors

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TLDR
The data support the hypothesis of an enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal axis in PTSD and combat veterans with PTSD suppressed cortisol to a greater extent than did combat veterans without PTSD and normal controls in response to both doses of dexamethasone.

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The data support earlier studies showing that HPA abnormalities in PTSD are different from those seen in depression and suggest that the low-dose dexamethasone suppression test may be a potentially useful tool for differentiating the two syndromes and further exploring differences in their pathophysiology.

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