Abstract
Evidence shows that Posttraumatic Stress Disorder (PTSD) patients have low basal cortisol levels and Glucocorticoid-Receptor (GR) super sensitivity following a pharmacological challenge. These findings, however, are controversial, partially due to the presence of confounding factors such as comorbidity with Major Depressive Disorder (MDD) and childhood trauma. In the present study, salivary cortisol levels of victims of violence with and without PTSD were assessed following a Prednisolone Suppression Test (PST), controlling for the presence of MDD and sexual abuse during childhood. The sample was nested in an epidemiological study performed in the city of Sao Paulo. Subjects with a diagnosis of PTSD (PTSD+) and a matched control group (PTSD-) were submitted to the Structured Clinical Interview for DSM-IV, after which the Early Trauma Inventory (ETI), Clinician-Administered PTSD Scale (CAPS), Beck Depression (BDI) and Anxiety Inventory (BAI) and Peri-traumatic Dissociative Experiences Questionnaire (PDEQ) were used. A saliva sample was collected before and after 5 mg of prednisolone was administered at 10 PM. Of the 34 PTSD+ patients, 19 had MDD comorbidity (PTSD+MDD). The cortisol curve of PTSD+MDD patients was similar to that of controls, and both were higher than that of PTSD patients. Cortisol levels after awakening after prednisolone administration were negatively correlated with the CAPS, BAI, and sexual abuse score on the ETI. These findings not only reinforce the idea that PTSD patients have GR super sensitivity, they also reveal that factors such as sexual abuse during childhood and comorbid MDD should be considered when studying HPA-axis reactivity, given their significant impact on the stress response.
Highlights
Posttraumatic Stress Disorder (PTSD) is a highly prevalent disorder [1], and diagnosis requires the presence of a stressor event that threatened the person’s emotional or physical integrity [2].Studies of the Hypothalamic-Pituitary-Adrenal (HPA) axis and autonomic nervous system are critical because they establish a relationship between the body/mind and the environment
The general linear model (GLM) regression showed a negative correlation between salivary cortisol levels after awakening and Clinician-Administered PTSD Scale (CAPS) (-.0069; se = .0016; p = .00021), BAI, (-.0094; se = .0035; p = .01199) and Early Trauma Inventory (ETI) (-.7222; se = .3792; p = .06616) scores; higher clinical scores were associated with lower cortisol concentrations after awakening. These results confirmed previous findings that PTSD patients have a blunted response to exogenous GC, which is likely due to increased GR and Mineralocorticoid Receptor (MR) responsiveness
It is important to reiterate that control subjects were exposed to traumatic events, which reinforces the fact that the HPA axis dysfunction is specific to PTSD development
Summary
Posttraumatic Stress Disorder (PTSD) is a highly prevalent disorder [1], and diagnosis requires the presence of a stressor event that threatened the person’s emotional or physical integrity [2].Studies of the Hypothalamic-Pituitary-Adrenal (HPA) axis and autonomic nervous system are critical because they establish a relationship between the body/mind and the environment. Posttraumatic Stress Disorder (PTSD) is a highly prevalent disorder [1], and diagnosis requires the presence of a stressor event that threatened the person’s emotional or physical integrity [2]. Acute stressors activate the HPA axis, studies of combat veterans, Holocaust survivors, refugees, and abused subjects, all of whom have been diagnosed with PTSD, reveal a paradoxical decrease in urine or blood cortisol levels compared to healthy controls and other diagnostic groups [3]. While this counterintuitive finding has been replicated, other findings have not been as consistent [4]. Differences in the type and timing of the psychological trauma, as well as symptom patterns, the presence of comorbid conditions, personality type, and genetic disposition (among other factors) may contribute to this inconsistency [4]
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