Citation

McFarlane AC, Barton CA, Yehuda R, Wittert G. Psychoneuroendocrinology 2011; 36(5): 720-727.

Affiliation

Centre for Military and Veterans Health, School of Population Health and Clinical Practice, The University of Adelaide, South Australia, Australia.

Copyright

(Copyright © 2011, Elsevier Publishing)

DOI

10.1016/j.psyneuen.2010.10.007

PMID

21093988

Abstract

This study sought to characterize the variability of the acute cortisol response following trauma and its relationship to posttraumatic stress disorder (PTSD). Forty eight participants were recruited within 24h of a traumatic accident requiring hospital admission. A saliva sample was collected at 08.00h and 16.00h 2 days, 1 month and 6 months after hospital admission, together with 24-h urine collection. Participants completed a dexamethasone suppression test (0.5mg DEX at 21.00h) at each follow up, together with self-report questionnaires. The Clinician Administered PTSD Scale (CAPS) was administered at 1 and 6 months to identify PTSD. Prevalence of PTSD was 27% at 1 month and 21% at 6 months. PTSD symptoms at 6 months were negatively correlated with salivary cortisol at 08.00h on day 2 (r=-0.36, p=0.04), but positively correlated with 16.00h cortisols (r=0.41, p=0.03). A lower rise in cortisol at 08.00h on day 2 was associated with an increase in risk of PTSD at both 1 month (OR=1.411 (1.017, 1.957)) and 6 months (OR=1.411 (1.066, 1.866)). At 1 month, 70% of participants with PTSD suppressed cortisol to more than 90% of pre-dex levels compared with 25% without PTSD (χ(2)=6.77, p=0.034). Urinary cortisol excretion was not different between groups at any time point. The findings support a hypothesis that sensitization of the HPA axis and enhanced suppression of cortisol following the dexamethasone suppression test are established early in the disease process.

Language: en