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Abstract <p>Many patients with major depressive disorder (MDD) have a concomitant history of traumatic exposure, and a substantial proportion develops comorbid post-traumatic stress disorder (PTSD). Comorbid PTSD worsens therapeutic response, occupational performance, interpersonal relationships, daily functioning, and quality of life. The biological mechanisms underlying these effects remain unclear. Aim of the study was identify PTSD related biochemical characteristics in patients with MDD. In a case control design, 95&#xa0;MDD patients with comorbid PTSD and 95 age matched MDD patients without PTSD were enrolled. Cases and controls were comparable in basic socio‑demographic variables and exhibited similar levels of biochemical indices, vitamins B9 andB12, pituitary hormones (adrenocorticotropic hormone, prolactin), and C‑reactive protein (CRP). Compared with MDD patients without PTSD, those with comorbid PTSD exhibited significantly elevated plasma cortisol and brain‑derived neurotrophic factor concentrations, significantly reduced 5‑dehydroepiandrosterone sulfate (5‑DHEA‑S) levels, and an approximately two‑fold increase in the cortisol/5‑DHEA‑S ratio. Spearman‑rank analysis demonstrated that a higher cortisol/5‑DHEA‑S ratio was modestly associated with poorer cognitive performance the Mini-Mental State Examination (MMSE) in both cohorts. In the MDD+PTSD subgroup, stronger relationships emerged: MMSE and State-Trait Anxiety Inventory-state (STAI-s) scores correlated positively with neutrophil counts, while MMSE scores correlated negatively with lymphocyte counts and STAI-s scores showed a weaker negative correlation with lymphocytes. Additionally, CRP levels were positively linked to neutrophil counts. These associations were absent in MDD patients without PTSD. These findings enhance insight into how dysregulated steroid hormones, altered neurotrophin levels, and inflammatory markers collectively contribute to the pathophysiology of comorbid PTSD in individuals with major depressive disorder.</p>

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Factors Associated with Posttraumatic Stress Disorder in Patients with Major Depressive Disorder

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月1日

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  • M. S. Zinchuk,
  • T. A. Druzhkova,
  • I. N. Mishin,
  • M. Yu. Zhanina,
  • S. B. Popova,
  • A. B. Guekht,
  • N. V. Gulyaeva

摘要

Abstract

Many patients with major depressive disorder (MDD) have a concomitant history of traumatic exposure, and a substantial proportion develops comorbid post-traumatic stress disorder (PTSD). Comorbid PTSD worsens therapeutic response, occupational performance, interpersonal relationships, daily functioning, and quality of life. The biological mechanisms underlying these effects remain unclear. Aim of the study was identify PTSD related biochemical characteristics in patients with MDD. In a case control design, 95 MDD patients with comorbid PTSD and 95 age matched MDD patients without PTSD were enrolled. Cases and controls were comparable in basic socio‑demographic variables and exhibited similar levels of biochemical indices, vitamins B9 andB12, pituitary hormones (adrenocorticotropic hormone, prolactin), and C‑reactive protein (CRP). Compared with MDD patients without PTSD, those with comorbid PTSD exhibited significantly elevated plasma cortisol and brain‑derived neurotrophic factor concentrations, significantly reduced 5‑dehydroepiandrosterone sulfate (5‑DHEA‑S) levels, and an approximately two‑fold increase in the cortisol/5‑DHEA‑S ratio. Spearman‑rank analysis demonstrated that a higher cortisol/5‑DHEA‑S ratio was modestly associated with poorer cognitive performance the Mini-Mental State Examination (MMSE) in both cohorts. In the MDD+PTSD subgroup, stronger relationships emerged: MMSE and State-Trait Anxiety Inventory-state (STAI-s) scores correlated positively with neutrophil counts, while MMSE scores correlated negatively with lymphocyte counts and STAI-s scores showed a weaker negative correlation with lymphocytes. Additionally, CRP levels were positively linked to neutrophil counts. These associations were absent in MDD patients without PTSD. These findings enhance insight into how dysregulated steroid hormones, altered neurotrophin levels, and inflammatory markers collectively contribute to the pathophysiology of comorbid PTSD in individuals with major depressive disorder.