EFFECTS OF ANTI-IL-17 THERAPY ON SERUM RED CELL DISTRIBUTION WIDTH AND MEAN PLATELET VOLUME IN ANKYLOSING SPONDYLITIS: A RETROSPECTIVE COHORT STUDY

Emrah KOÇ, Suade Özlem BADAK

Çukurova Anestezi ve Cerrahi Bilimler Dergisi - 2026;9(2):340-348

Department of Rheumatology, Adana City Training and Research Hospital, Adana, Türkiye

 

Objective: To investigate the effects of anti-IL-17 therapy on serum red cell distribution width (RDW) and mean platelet volume (MPV) in patients with ankylosing spondylitis (AS) and to evaluate their relationship with disease activity markers. Methods: This retrospective cohort study included 130 AS patients (86 males, 44 females; mean age 35.7 +/- 8.9 years) receiving anti-IL-17 inhibitors (secukinumab or ixekizumab). Pre-treatment and post-treatment (mean 21.4 +/- 19.0 months) RDW, MPV, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were recorded. Paired t-tests with Bonferroni correction, Pearson correlation analyses, and multiple linear regression analyses were performed. Results: Anti-IL-17 therapy resulted in significant reductions in RDW (15.43 +/- 0.79 vs. 14.60 +/- 0.83%, p < 0.001; Cohen's d = 2.94), MPV (10.46 +/- 0.71 vs. 10.16 +/- 0.74 fL, p < 0.001; Cohen's d = 1.48), BASDAI (6.53 +/- 1.27 vs. 3.30 +/- 1.51, p < 0.001; Cohen's d = 4.28), ESR (27.19 +/- 12.27 vs. 15.29 +/- 12.23 mm/h, p < 0.001), and CRP (17.42 +/- 9.26 vs. 9.21 +/- 8.72 mg/L, p < 0.001). Good clinical response (>=50% BASDAI reduction) was achieved in 48.5% of patients. Pre-treatment RDW correlated significantly with BASDAI (r = 0.33, p < 0.001), ESR (r = 0.45, p < 0.001), and CRP (r = 0.42, p < 0.001). Conclusion: Anti-IL-17 therapy effectively suppresses disease activity and systemic inflammation in AS patients. The significant reductions in RDW and MPV alongside clinical and inflammatory markers suggest that these readily available hematologic parameters might serve as adjunctive, hypothesis-generating biomarkers for monitoring treatment response and systemic inflammation in AS.