Dose-Response Changes in Plasma Cortisol and Lymphocyte Glucocorticoid Receptors Following Dexamethasone Administration in Combat Veterans With and Without Posttraumatic Stress Disorder

doi:10.1001/archpsyc.1995.03950190065010

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Vol. 52 No. 7, July 1995

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Dose-Response Changes in Plasma Cortisol and Lymphocyte Glucocorticoid Receptors Following Dexamethasone Administration in Combat Veterans With and Without Posttraumatic Stress Disorder

Rachel Yehuda, PhD; David Boisoneau; Martin T. Lowy, PhD; Earl L. Giller, Jr, MD, PhD

Arch Gen Psychiatry. 1995;52(7):583-593.

Abstract

Background
Our previous studies have suggested that combat veterans withposttraumatic stress disorder (PTSD) have alterations in hypothalamic-pituitary-adrenalaxis functioning that are different from the well-documentedbiological changes observed in major depressive disorder andfollowing exposure to stress.

Methods
In the present study, we examined cortisol and lymphocyte glucocorticoidreceptor number before and after the administration of 0.50and 0.25 mg of dexamethasone in 14 combat veterans with PTSD,12 combat veterans without PTSD, and 14 nonpsychiatric healthymen. All subjects were medication free at the time of testingand none met diagnostic criteria for major depression or substancedependence.

Results
Combat veterans with PTSD suppressed cortisol to a greater extentthan did combat veterans without PTSD and normal controls inresponse to both doses of dexamethasone. Differences in cortisolsuppression could not be attributed to substance dependencehistory or differences in dexamethasone bioavailability. Combatveterans with PTSD showed a larger number of baseline glucocorticoidreceptors compared with normal men. Combat veterans withoutPTSD also had a larger number of baseline glucocorticoid receptorscompared with normal men and in fact were comparable to combatveterans with PTSD on this measure. However, only veterans withPTSD showed a decrease in lymphocyte glucocorticoid receptornumber following dexamethasone administration.

Conclusion
The data support the hypothesis of an enhanced negative feedbacksensitivity of the hypothalamic-pituitary-adrenal axis in PTSD.

Author Affiliations

From the Departments of Psychiatry, Mount Sinai School of Medicine and Bronx Veterans Affairs Medical Center, New York, NY (Dr Yehuda), and University of Connecticut Health Center, Farmington (Mr Boisoneau); the Burroughs Wellcome Co, Research Triangle Park, NC (Dr Lowy), and CNS Research, Pfizer Inc, Groton, Conn (Dr Giller).

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