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Abstract
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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.
Language: en |