Background: Post-traumatic stress disorder (PTSD) is a severe psychiatric condition prevalent among combat veterans. Its diagnosis is challenging due to the heterogeneity of clinical presentations and the complex interplay of pathogenic factors. Objective: This study aimed to develop and validate a diagnostic algorithm for combat-related PTSD by integrating clinical data with a panel of biological markers associated with blood–brain barrier disruption (anti-GFAP and anti-NSE antibodies), HPA axis dysfunction (cortisol), and neuroinflammation (IL-6, IL-8). Methods: A total of 721 male participants were enrolled: 434 veterans with PTSD (F43.1), 147 combat veterans without PTSD, and 140 non-combat military controls. All participants underwent clinical and psychometric assessment (Likert scale, HADS). Serum levels of biomarkers were measured using ELISA. Statistical analysis included non-parametric tests, correlation analysis, and binary logistic regression with Wald’s method to build a predictive model. Results: The binary logistic regression model identified cortisol and IL-6 as the most significant predictors of PTSD. The final algorithm, based on a cortisol level below 199.8 nmol/L and an IL-6 level above 0.002438 pg/mL, correctly classified 78% of patients (AUC = 0.724, 95% CI [0.669, 0.779]). Furthermore, levels of IL-4, IL-8, and cortisol positively correlated with the severity of combat stress factors, independent of physical injuries. Conclusions: We developed a novel diagnostic algorithm for combat-related PTSD based on cortisol and IL-6 levels, demonstrating high accuracy. The correlation between neuroinflammatory markers and the severity of combat exposure suggests their role as primary indicators of stress response, highlighting their utility for early risk identification and targeted interventions.

Post-traumatic stress disorder (PTSD) is a mental health condition that can arise following exposure to deeply upsetting events, such as violence, natural disasters, military conflicts, or situations posing a threat to one's life. Although our knowledge of PTSD mechanisms has expanded, therapeutic approaches remain challenging, due to the diverse symptoms profile and the limited benefit of current treatment strategies of PTSD. Recent studies have documented an interaction between coping strategies and the development of PTSD. The current review aims to provide the available evidence for the impact of coping strategies in the development and treatment of PTSD. The present results indicate that coping strategies have an important role in the pathogenesis and treatment of PTSD. Adaptive strategies increase resilience and facilitate recovery, while maladaptive strategies contribute to chronicity and treatment resistance. However, the relationships observed between cognitive coping strategies and PTSD outcomes have remained under discussion. The next investigations with focus on a combination of pharmacotherapy with different coping strategies could be a beneficial for personalized therapy of PTSD.

Objective: To investigate changes in serum neuroinflammatory biomarker concentrations and associated psychopathological manifestations in individuals with post-traumatic stress disorder, taking into account the presence or absence of traumatic brain injury. Methods: The study involved 159 male combat veterans who had been involved in combat within the year prior to their inclusion in the study, divided into four groups: veterans without post-traumatic stress disorder or traumatic brain injury ( n = 43), veterans without post-traumatic stress disorder but with traumatic brain injury ( n = 41), veterans with post-traumatic stress disorder but without traumatic brain injury ( n = 38), and veterans with both post-traumatic stress disorder and traumatic brain injury ( n = 37). Psychometric parameters (subjective stress severity, depression, avoidance, hyperarousal, intrusive thoughts, and alterations in personality traits) were evaluated. Serum concentrations of antibodies to glial fibrillary acidic protein and neuron-specific enolase were assessed using enzyme-linked immunosorbent assay, while YKL-40, migration inhibitory factor, receptor for advanced glycation end-products, interleukin-34, B-lymphocyte chemoattractant, and triggering receptor expressed on myeloid cells 2 were measured using multiplex assays. Results: Traumatic brain injury presence was associated with reduced severity of depression and avoidance symptoms compared to individuals with post-traumatic stress disorder alone. Elevated serum levels of glial fibrillary acidic protein and neuron-specific enolase antibodies were observed in post-traumatic stress disorder patients, with neuron-specific enolase antibodies particularly increased in the post-traumatic stress disorder + traumatic brain injury group. Notably, YKL-40 levels were decreased in the post-traumatic stress disorder + traumatic brain injury group. Migration inhibitory factor concentration was reduced in post-traumatic stress disorder, while isolated post-traumatic stress disorder was linked to higher receptor for advanced glycation end-products levels. Significant correlations were found between biomarker concentrations and psychometric indices. Conclusion: The findings reveal distinct clinical and biochemical profiles for isolated post-traumatic stress disorder and post-traumatic stress disorder comorbid with traumatic brain injury, reflecting differences in underlying pathophysiological processes. The data suggest involvement of neuroinflammation, blood–brain barrier disruption, and autoimmune mechanisms in post-traumatic stress disorder pathogenesis—particularly when traumatic brain injury is also present. Identified biomarkers may enhance diagnostic and prognostic tools in combat psychiatry.