AI Summary & Key Takeaways
AI InsightSerum 25(OH)D levels were inversely correlated with CRP (r=-0.304, p=0.002) and BASDAI (r=-0.335, p=0.001) in the overall cohort.
📌 3 Key Takeaways
Abstract
Aim This study aims to evaluate the association between serum 25-hydroxyvitamin D [25(OH)D] levels and inflammatory markers as well as disease activity in patients with ankylosing spondylitis (AS) receiving biologic therapy, including TNF inhibitors, IL-17 inhibitors, and JAK inhibitors. Material and Methods This cross-sectional study includes 104AS patients receiving biologic therapy for at least six months. Patients were categorized based on serum 25(OH)D levels: deficiency ( 30 μg/L). Disease activity was assessed using Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Bath Ankylosing Spondylitis Functional Index (BASFI) scores. Laboratory parameters, including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured. Group comparisons are performed using the Kruskal–Wallis test or one-way ANOVA, as appropriate, and the Chi-square test for categorical variables. Correlations between serum 25(OH)D levels and clinical or laboratory parameters are evaluated using Spearman’s rank correlation analysis. Subgroup analyses are conducted according to biologic treatment class. Results Patients with vitamin D deficiency had significantly higher CRP levels (24.0 mg/L vs. 12.1 mg/L vs. 8.9 mg/L, p=0.001), elevated ESR (p=0.028), and higher BASDAI scores (8.0 vs. 6.7 vs. 5.3, p<0.001) compared to those with insufficiency and sufficiency. Serum 25(OH)D levels were inversely correlated with CRP (r=-0.304, p=0.002) and BASDAI (r=-0.335, p=0.001) in the overall cohort. Subgroup analyses revealed significant negative correlations between 25(OH)D and CRP (r=-0.426, p<0.001) and BASDAI (r=-0.317,p=0.008) in TNF inhibitor-treated patients, and between 25(OH)D and BASDAI (r=-0.609, p=0.001) in IL-17 inhibitor-treated patients. Conclusion Lower serum 25(OH)D levels are significantly associated with higher inflammatory markers and increased disease activity in biologic-treated AS patients. These findings suggest that vitamin D deficiency may be associated with increased inflammatory burden and disease activity in biologic-treated AS patients. Future prospective and interventional studies are needed to determine whether vitamin D supplementation improves clinical outcomes in this population.