Current status of cortisol findings in post-traumatic stress disorder
ABSTRACT This article summarizes findings of hypothalamic-pituitary-adrenal axis alterations in post-traumatic stress disorder (PTSD) and evaluates likely reasons for the lack of agreement among published studies. Sources of variance caused by methodologic and interpretative differences are highlighted, but the disparate findings are explained as illustrating a more complex neuroendocrinology of PTSD than has previously been described.
SourceAvailable from: Marit Sijbrandij[Show abstract] [Hide abstract]
ABSTRACT: Background An increasing number of studies have investigated the pharmacological prevention of post-traumatic stress disorder (PTSD) and acute stress disorder (ASD). This is the first systematic review to examine the effects of pharmacotherapies (eg, β blockers, hydrocortisone, and selective serotonin re-uptake inhibitors) given within the first month after a traumatic or aversive event to prevent PTSD or ASD compared with no pharmacotherapy or placebo control. Methods A systematic literature search in PubMed, PsycINFO, Embase, and the Cochrane database of randomised trials was done. Studies included randomised controlled trials, controlled clinical trials, and cohort studies; their overall quality was low to moderate. We computed the pooled incidence risk ratio (IRR): the risk of incidence of PTSD or ASD in the pharmacotherapy groups relative to the incidence of PTSD or ASD in the control groups. Additionally, we computed Hedges' g effect sizes for PTSD or ASD continuous outcomes. Findings 15 studies met inclusion criteria (1765 individuals). Pharmacotherapy was more effective in preventing PTSD or ASD than placebo or no intervention (14 studies, 1705 individuals, IRR 0·65, 95% CI 0·55–0·78; number needed to treat 11·36), although no effect was found when only randomised controlled trials were included (ten studies, 300 individuals, IRR 0·69, 95% CI 0·40–1·21). Hydrocortisone showed a large effect in reducing the risk of PTSD (five studies, 164 individuals, IRR 0·38, 95% CI 0·16–0·92). Interpretation No firm evidence was found for the efficacy of all early pharmacotherapies in the prevention of PTSD or ASD, but hydrocortisone reduced the risk of developing PTSD. The small number of studies and their limited methodological quality cast uncertainty about the effects. Funding None.The Lancet Psychiatry 04/2015; DOI:10.1016/S2215-0366(14)00121-7
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ABSTRACT: The aim of this study was to determine whether there is increased responsiveness to corticosteroids in posttraumatic stress disorder (PTSD) by examining the differential effects of dexamethasone (DEX) on the inhibition of lysozyme activity.Methods60 mL of blood was withdrawn at 8:00 am, and mononuclear leukocytes were isolated from the blood of 26 men with, and 18 men without, PTSD. An aliquot of live cells was incubated with a series of concentrations of DEX to determine the rate of inhibition of lysozyme activity; a portion of cells was frozen for the determination of glucocorticoid receptors (GR).ResultsSubjects with PTSD showed evidence of a greater sensitivity to glucocorticoids as reflected by a significantly lower mean concentration (nmol/L) of dexamethasone at which 50% of lysozyme activity is inhibited (IC50-DEX) (PTSD+ = 4.9 ± .53; PTSD− group = 7.2 ± .64). The lysozyme IC50-DEX was significantly correlated with age at exposure to the first traumatic event in subjects with PTSD (r = .44, n = 26, p = .025). The number of cytosolic glucocorticoid receptors was also correlated with age at exposure to the focal traumatic event (r = −.44, n = 25, p = .03) in PTSD.Conclusions This is the first in vitro demonstration of an alteration in target tissue sensitivity to glucocorticoids in PTSD. The lower lysozyme IC50-DEX might be related to the risk factor of prior exposure to trauma.Biological Psychiatry 06/2004; 55(11):1110-1116. DOI:10.1016/S0006-3223(04)00188-X · 9.47 Impact Factor