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Posttraumatic stress disorder (PTSD) and depression severity in sexually assaulted women: hypothalamic-pituitary-adrenal (HPA) axis alterations

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Ana Teresa D D'Elia, Mario F Juruena, Bruno M Coimbra, Marcelo F Mello, Andrea F Mello

Original languageEnglish
Article number174
Pages (from-to)174
Number of pages1
JournalBMC Psychiatry
Volume21
Issue number1
DOIs
Published31 Mar 2021

Bibliographical note

Funding Information: This research was supported by grants from FAPESP 2014/12559–5 and CNPq 303389/2016–8, and financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) - Finance Code 001. The funders had no role in the design of the study and collection, analysis, interpretation of data and in writing the manuscript. Funding Information: Dr. Marcelo F. Mello is supported by Scholarship CNPq (303389/2016–8), funded by FAPESP (grant 2014/12559–5). Dr. Mario F. Juruena is a Consultant at South London and Maudsley NHS Foundation Trust (SLaM-NHS UK) supported by the National Institute for Health Research (NIHR); Biomedical Research Centre (BRC) a partnership of South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London; and is Senior Clinical Lecturer at King’s College London. MF Juruena has within the last year received honoraria for speaking from Lundbeck, Janssen, Livanova and Daiichi Sankyo. Ana Teresa D′ Elia, Bruno M. Coimbra and Dr. Andrea F. Mello declare that they have no conflicts of interest. Publisher Copyright: © 2021, The Author(s). Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

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Abstract

BACKGROUND: Sexual assault is implicated in several adverse psychological and physical health outcomes, including posttraumatic stress disorder (PTSD) and depression. Neurobiological research has shown variations related to the hypothalamic-pituitary-adrenal (HPA) axis, immune alterations, metabolic function, and brain circuitry. Although these mechanisms have been extensively studied, the results have demonstrated different outcomes in PTSD. METHODS: We compared the plasma adrenocorticotropin (ACTH) and salivary cortisol levels of fifty-eight women with PTSD developed after sexual assault to those of forty-four female controls with no history of trauma. We also evaluated the psychiatric diagnosis and symptom severity of PTSD and depression. The participants' clinical conditions were associated with their hormonal levels to assess whether symptom severity was related to hormonal imbalance. RESULTS: A large percentage of sexually assaulted women had PTSD and comorbid depression. The ACTH levels were higher in the PTSD group than the control group and increased as PTSD severity increased, considering depressive symptoms, measured by the Beck Depression Inventory (BDI) (p < 0.0001), as well as PTSD symptoms, measured by subscale D of the Clinician-Administered PTSD Scale (CAPS-5) (p = 0.045) and the CAPS-5 total scale (p = 0.026). Cortisol levels measured at 10 pm were higher for the PTSD group than the control group (p = 0.045, p = 0.037, respectively), and the cortisol awakening response showed elevated cortisol levels for the PTSD group. CONCLUSIONS: These results show a correlation between symptom severity and HPA axis imbalance in patients with PTSD. Elevated ACTH and an elevated cortisol response in patients with comorbid depressive symptoms were the opposite of the expected response for patients with PTSD only. This association leads to the hypothesis that the neurobiological alterations of PTSD are related to the type of symptoms presented and their severity. These manifestations likely influence the disease course, prognosis and response to treatment. These outcomes highlight the need to discuss particular neurobiological alterations in patients with PTSD developed after sexual assault, mainly those with severe depressive symptoms.

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