Akademik Veri Yönetim Sistemi
Psychoneuroendocrinology, cilt.188, 2026 (SCI-Expanded, Scopus)
Background While systemic inflammation is the hallmark of Systemic Lupus Erythematosus (SLE) and Sjögren’s Syndrome (SS), the failure of endogenous "anti-inflammatory brakes" remains poorly understood. The Hypothalamic-Pituitary-Adrenal (HPA) axis and the Autonomic Nervous System (ANS) constitute the body’s primary neuro-immune regulatory circuit. This study investigates whether concurrent dysregulation of these two systems contributes to the persistent inflammatory state in SLE and SS. Methods In this cross-sectional study, we evaluated 40 patients with Systemic Lupus Erythematosus (SLE), 40 with Sjögren’s Syndrome (SS), and 32 age- and sex-matched healthy controls. Cardiac autonomic modulation was quantified via Heart Rate Variability (HRV) analysis using short-term (5-minute) ECG recordings. The dynamic activity of the hypothalamic-pituitary-adrenal (HPA) axis was mapped through the Cortisol Awakening Response (CAR), utilizing salivary samples collected at four precise time points (awakening, +30 min, +60 min, and bedtime) and analyzed via ELISA. To ensure protocol reliability, only samples from participants with verified spontaneous awakening were included. Systemic inflammation was assessed through hemogram parameters and serum C-reactive protein (CRP, mg/dL) levels. Results Our data reveal a distinctive neuroendocrine-immune signature in both disorders. Both SLE and SS patients exhibited a significantly blunted CAR at 60 min (p < 0.05), suggesting a failure in the "anticipatory" stress response. Autonomic profiling showed widespread impairment in SDNN and Total Power (p < 0.05) across both groups. Notably, we identified a phenotypic divergence: SLE patients demonstrated a specific impairment in parasympathetic "vagal tone" (RMSSD and HF), whereas SS patients were characterized by a unique leukocyte and neutrophil depletion (p < 0.05). This suggests that while HPA hyporesponsiveness is a shared trait, the autonomic-immune coupling may follow disease-specific pathways. Conclusions This study provides compelling evidence of interrelated regulatory alterations in the neuro-immune axis of SLE and SS patients. The combination of diminished cortisol signaling and impaired vagal modulation creates a "permissive environment" for chronic inflammation. By demonstrating that the degree of HPA suppression correlates with autonomic rigidity, we propose a new theoretical framework: systemic autoimmunity is not merely an immune defect but a dysregulation of the neuroendocrine-autonomic homeostatic loop. Targeting this "stress-axis" could provide a novel bio-behavioral window for therapeutic intervention and disease monitoring.