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Increased immuno-inflammatory mediators in women with post-traumatic stress disorder after sexual assault: 1-Year follow-up

Research output: Contribution to journalArticlepeer-review

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

Original languageEnglish
Pages (from-to)241-251
Number of pages11
JournalJournal of psychiatric research
Early online date13 Sep 2022
Accepted/In press31 Aug 2022
E-pub ahead of print13 Sep 2022
PublishedNov 2022

Bibliographical note

Funding Information: This research was supported by grants from FAPESP 2014/12559-5 and CNPq 303389/2016-8 . 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 funded by the Biomedical Research Center (BRC) , a partnership of South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) 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: © 2022 Elsevier Ltd

King's Authors


Background: Sexual violence is a traumatic event that can trigger post-traumatic stress disorder (PTSD) and generate biological responses to stress characterized by inhibiting the hypothalamic-pituitary axis (HPA), altering immune activity, and changing the structure and function of the brain. PTSD is associated with increased levels of inflammatory markers. This study aimed to measure differences in inflammatory markers and HPA hormone levels between women with PTSD due to sexual violence and controls at baseline and after 1-year follow-up. Methods: Fifty-eight women with PTSD resulting from sexual assault occurring up to 6 months prior were compared to 41 female controls. The patients were followed for 1 year. At baseline (T1), we measured inflammatory biomarkers. We also applied the Mini International Neuropsychiatric Interview (MINI), the Clinician-Administered Post-Traumatic Stress Disorder Scale-5, the Beck Depression Inventory, the Beck Anxiety Inventory, and the Childhood Trauma Questionnaire. The patients were randomized to receive treatment with sertraline or interpersonal psychotherapy for 14 weeks (T2) and then continued the usual treatment if deemed necessary for 1 year. The same interviews and examinations were repeated after 1 year (T3). Results: At baseline, the patients had significantly higher adrenocorticotropic hormone levels, compared to controls; however, there was no baseline difference in inflammatory markers or cortisol. After 1 year, there were significantly higher levels of interleukin-1β (p < 0.0001), monocyte chemoattractant protein-1 (p < 0.0001), tumor necrosis factor-α (p < 0.0001), c-reactive protein (p < 0.0001), and cortisol (p = 0.046) in the patient group. In addition to PTSD, 56 patients presented with a major depressive episode at T1 (according to the MINI). At the end of 1 year, there was a significant improvement in depressive (p < 0.001), anxiety (p = 0.03), and PTSD symptoms (p < 0.001) regardless of the treatment received. Discussion: The increase of the inflammatory markers after 1 year, even with symptomatic improvement, may indicate that PTSD following sexual violence is associated with high depressive symptoms. This association may have a different pattern of immunoendocrine alterations than PTSD only. Furthermore, these alterations may persist in the long term, even with the improvement of the symptoms, probably generating an immunological imprint that can lead to future clinical consequences. This study adds to the current knowledge of PTSD neurobiology and contributes to broadening approaches to this disorder.

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