@article{ref1,
title="Cortisol response to acute trauma and risk of posttraumatic stress disorder",
journal="Psychoneuroendocrinology",
year="2011",
author="McFarlane, Alexander C. and Barton, Christopher A. and Yehuda, Rachel and Wittert, Gary",
volume="36",
number="5",
pages="720-727",
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.<p /> <p>Language: en</p>",
language="en",
issn="0306-4530",
doi="10.1016/j.psyneuen.2010.10.007",
url="http://dx.doi.org/10.1016/j.psyneuen.2010.10.007"
}