Assessment of Galectin-3, S100B, thiol/thiol disulphide and ischemia-modified albumin levels in children and adolescents with post-traumatic stress disorder

Aim: Post-Traumatic Stress Disorder (PTSD) is one of the common psychiatric disorders following trauma in children and adolescents. This condition, which adversely affects quality of life, results in a high medical and socioeconomic burden. This study aimed to compare the levels of Galectin-3 (a potential marker of neuroinflammation), S100B (a neuronal damage marker), thiol/disulfide homeostasis (indicating oxidative stress), and ischemia-modified albumin (IMA) between PTSD patients and a healthy control group, and to examine their association with symptom severity and clinical features. Methods: The study included 44 female children and adolescents diagnosed with PTSD following sexual abuse who presented to our Child and Adolescent Psychiatry Outpatient Clinic, along with 44 age- and sex-matched healthy controls. Although the planned inclusion age range was 8–17 years, the study was completed with participants aged 12–17 years. The Screen for Child Anxiety Related Disorders, the Children's Depression Inventory, the Childhood Trauma Questionnaire, the Child Post-Traumatic Stress Reaction Index, and the Clinical Global Impression–Severity Scale (CGI-S) were administered. Venous blood samples collected from participants were transported under appropriate conditions to the Medical Biochemistry Laboratory of Ankara Bilkent City Hospital. Serum Galectin-3 and S100B levels were measured using ELISA, thiol/disulfide homeostasis was assessed via the fully automated spectrophotometric method developed by Erel and Neşelioğlu, and IMA levels were analyzed using the albumin–cobalt binding test described by Bar-Or et al. Results: S100B and IMA levels were significantly higher in the PTSD group compared with controls, whereas native thiol, total thiol, and disulfide levels were significantly lower. ROC analysis demonstrated that IMA showed high diagnostic performance in distinguishing PTSD, with a sensitivity of 81.4% and a specificity of 81.8%. No significant difference was observed between groups in terms of Galectin-3 levels. The PTSD group exhibited higher neutrophil percentages and lower lymphocyte percentages and counts. Red blood cell count and hemoglobin levels were lower, whereas fasting glucose levels were higher in the PTSD group. Galectin-3 levels were positively correlated with CGI-S scores, indicating that increased Galectin-3 was associated with greater clinical severity. Conclusion: The findings of this study demonstrate that neuroinflammation and oxidative stress play an important role in the pathophysiology of PTSD. Elevated IMA levels and reduced thiol parameters support increased oxidative burden and reduced antioxidant capacity. The high diagnostic performance of IMA suggests that it may serve as a promising biomarker for PTSD. The association between Galectin-3 levels and clinical severity further indicates its potential utility as an adjunct marker in monitoring disease progression. Disruption of thiol–disulfide homeostasis, alterations in neutrophil/lymphocyte parameters, and metabolic abnormalities collectively support the notion that PTSD is a systemic disorder. These findings may contribute to the objective biological evaluation of PTSD and to the development of future treatment strategies.