DIAGNOSTIC SIGNIFICANCE OF CORTISOL AND β-ENDORPHIN IN THE DEVELOPMENT OF SOMATOVEGETATIVE SYNDROME IN CHRONIC CEREBRAL ISCHEMIA AND EFFECTIVENESS OF INDIVIDUALIZED THERAPY
Keywords:
chronic cerebral ischemia, somatoform autonomic dysfunction, cortisol, β-endorphin, COMPASS-31, HADS-A, PSS-10, alimemazine, TeraligenAbstract
Aim: to evaluate the clinical and laboratory significance of cortisol and β-endorphin in patients with somatoform autonomic dysfunction (SAD) against the background of stage I-II chronic cerebral ischemia (CCI), and to assess the efficacy of adding alimemazine (Teraligen) to standard therapy. Material and methods: the study included 64 patients with clinical signs of SAD on the background of stage I-II CCI (main group), 40 patients with CCI without signs of SAD (comparison group), and 30 practically healthy individuals (control group). All patients were assessed using the COMPASS-31, PSS-10, and HADS-A scales, and serum cortisol and β-endorphin concentrations were determined by ELISA. At the treatment stage, the main group was divided into two subgroups: 1a (n=33) — standard therapy plus alimemazine, and 1b (n=31) — standard therapy alone. Results: in the main group (mean age 49.8±2.1 years; 59.4% female), cortisol was 748.3±252.6 nmol/L, β-endorphin was 120.8±19.2 pg/mL, COMPASS-31 was 28.7±7.2 points, and HADS-A was 10.8±1.7 points; a high stress level was recorded in 57.8% of patients. Cortisol and β-endorphin showed moderate-to-strong positive correlations with COMPASS-31, HADS-A, and PSS-10 (ρ=0.45–0.68; p<0.05) and were independent predictors of SAD development (OR=1.009 and OR=1.007, respectively; p<0.05). At the end of treatment, group 1a showed reductions of 57.7% in COMPASS-31, 62.6% in PSS-10, 56.3% in HADS-A, 33.8% in cortisol, and 15.2% in β-endorphin (all p<0.001), whereas group 1b showed reductions of 21.0%, 39.0%, 23.1%, 11.8%, and a statistically non-significant 3.2%, respectively. Conclusion: cortisol and β-endorphin are reliable neurohumoral markers and independent predictors of SAD; adding alimemazine to standard therapy produces significantly greater improvement in clinical, psychometric, and neurohumoral indicators.
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