Features of the impact of thyroid gland dysfunction on neuron-specific enolase levels as a marker of neuronal changes

Aim. To study the influence of thyroid dysfunction on neuron-specific enolase (NSE) as a biochemical marker of neuronal damage associated with impaired thyroid hormone synthesis. Materials and methods. Serum samples from 51 participants were analyzed, including 18 patients with hypothyroidism, 18 patients with hyperthyroidism (both aged 28–47 years), and 15 healthy controls (aged 25–50 years). Serum concentrations of thyroid hormones (T3, T4), TSH, and NSE were measured using standard ELISA. Neurological manifestations were recorded from medical charts. Statistical comparisons between each patient group and the control group were performed using non-parametric methods (Mann–Whitney U test) due to small sample size and deviations from normality. Results. Hypothyroid patients exhibited significantly lower T3 (1.15 pg/mL) and T4 (0.77 ng/dL) and elevated TSH (7.5 mIU/L) compared with controls (T3 – 2.3 pg/mL; T4 – 1.7 ng/dL; TSH – 2.1 mIU/L). NSE was markedly elevated in hypothyroid patients (26.2 ng/mL) versus controls (6.0 ng/mL). Hyperthyroid patients showed elevated T3 (7.65 pg/mL), T4 (3.39 ng/dL), suppressed TSH (0.04 mIU/L), and elevated NSE (24.0 ng/mL) compared with controls. All measured parameters differed significantly from the corresponding control values (p < 0.001). Conclusions. Both hypothyroidism and hyperthyroidism are associated with significantly elevated NSE levels, suggesting neuronal involvement. NSE may serve as a sensitive biochemical marker of neuronal perturbation in thyroid dysfunction.