Akademik Veri Yönetim Sistemi
AKTUELLE RHEUMATOLOGIE, cilt.48, sa.02, ss.131-136, 2023 (SCI-Expanded)
Aim: More and more studies have demonstrated that the interleukin (IL)-23/IL-17 axis is highly associated with immune dysfunction and activated autoimmune inflammation. The purposes of this study were to determine the serum levels of IL-17 and IL-23 in ankylosing spondylitis (AS) patients compared with healthy controls and evaluate these cytokine levels based on disease-related characteristics. Material and Methods: Eighty-six consecutive AS patients and 70 sex and age-matched healthy controls were included in the study. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Ankylosing Spondylitis Disease Activity Score (ASDAS)-erythrocyte sedimentation rate (ESR), ASDAS-C reactive protein, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Spondyloarthrit is Research Consortium of Canada (SPARCC) enthesitis index, the Bath Ankylosing Spondylitis Metrology Index (BAS -MI), the Ankylosing Spondylitis Quality of Life Questionnaire (ASQoL) and Achilles pain VAS scores were recorded. Serum IL-17 and IL-23 levels were examined by enzyme-linked immunosorbent assay. Results: The serum levels of IL-17, IL-23 and CRP as well as ESR values were significantly increased in AS patients compared with controls (1.94 vs. 0.28 pg/mL p < 0.001; 82.9 vs. 44.3 pg/mL p < 0.001; 0.48 vs. 0.30 mg/dL, p = 0.001; 12 +/- 13.9 vs. 8 +/- 6.8 mm/h, p = 0.003, respectively). In AS patients, serum IL-17 levels were significantly correlated with the ASDAS-ESR and ASDAS-CRP (r = 0.244, p = 0.024; r = 0.258, p = 0.017), but not with ESR, CRP, BASDAI, function, mobility, quality of life, enthesitis index or Achilles pain scores (all p > 0.05). Serum IL-23 levels demonstrated a significant correlation with Achilles pain VAS, but not with other disease-related parameters (all p > 0.05). Conclusions: AS patients had increased serum IL-17 and IL-23 levels compared with healthy controls, and serum IL-17 levels were associated with disease activity. Our study results support the hypothesis that the IL17/23 pathway plays an important role in the pathogenesis of AS.