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Background: Reactive spondyloarthritis, classified as an autoimmune-autoinflammatory form of spondyloarthropathy, is often associated with infectious triggers and frequently develops in the middle-aged population. This condition significantly impacts patients’ quality of life and can lead to structural joint damage and early disability. Notably, spondyloarthritis encompasses not only ankylosing spondylitis but also reactive arthritis, psoriatic arthritis, and conditions associated with inflammatory bowel diseases. Interleukin-17A (IL-17A), a key cytokine playing a critical role in inflammatory processes, holds significant importance in the pathogenesis of autoimmune and inflammatory diseases. However, the specific role of IL-17A in reactive spondyloarthritis and its influence on disease severity remain inadequately studied. Therefore, a deeper investigation into the role of IL-17A in reactive spondyloarthritis is crucial for refining diagnostic approaches and therapeutic strategies.
Objectives: To evaluate the role of Interleukin-17A (IL-17A) in the pathogenesis and progression of reactive spondyloarthritis, as well as to assess its association with disease activity and the impact of biological DMARD (IL-17A inhibitor) through a 13-, 26-, and 52-week prospective study.
Methods: A total of 184 patients diagnosed with ReA were enrolled in the study, of which 112 were identified to have spondylitis. The age range of participants was 20–54 years, with a mean age of 32.3±10.2 years, and the average disease duration was 3.7±1.8 years. Among the patients, 132 (71.7%) were male, and 52 (28.3%) were female. Plasma IL-17A concentrations were measured using the enzyme-linked immunosorbent assay (ELISA) method, with follow-up evaluations conducted at weeks 13, 26, and 52. Disease activity, joint damage, enthesitis, and spinal involvement were assessed using ASDAS, MASES (Maastricht Ankylosing Spondylitis Enthesitis Score) and DAREA (Disease Activity in Reactive Arthritis) indices throughout the same time intervals.
Results: In healthy male participants, the baseline IL-17A level was 62.4±11.24 ng/mL, whereas in male patients, it significantly increased to 173.3±35.2 ng/mL (p>0.002). Similarly, in healthy females, the IL-17A level was 53.4±8.2 ng/mL, while in female patients, it reached 125.2 ± 32.8 ng/mL (p>0.05). When stratifying groups based on the presence of spondyloarthritis (ReA per se and ReSpA), marked differences in IL-17A levels were observed. In patients with ReSpA, the IL-17A level surged to 204.7 ± 44.5 ng/mL (p<0.0001), significantly higher than in healthy controls (62.4±11.24 ng/mL) and ReA per se patients (79.4 ± 38.1 ng/mL) respectively. Furthermore, IL-17A levels in ReSpA patients were noted to be 2.5 times higher compared to ReA per se. Analysis of IL-17A levels across disease stages revealed that chronic cases exhibited 246.7±62.1 ng/mL (p<0.05), prolonged cases 194.3±33.4 ng/mL (p<0.05), and acute cases 89.4±42.8 ng/mL (p>0.05). IL-17A levels were significantly elevated in chronic and prolonged cases compared to the control group, while no statistically significant difference was observed in acute cases. Etiologically, IL-17A levels were significantly higher in the genitourinary form for both genders compared to controls (p<0.001). In the gastrointestinal form, IL-17A levels were also statistically significant in males (p<0.001) and females (p<0.002). Male patients with the genitourinary form exhibited notably higher IL-17A levels than those with the gastrointestinal form (p<0.05). Correlation analysis revealed a weak negative association between IL-17A and the MASES and DAREA indices in ReA per se patients (MASES: r =0.06; DAREA: r =0.16). However, in ReSpA patients, IL-17A levels strongly and positively correlated with both indices (MASES: r =0.67; DAREA: r =0.55; p<0.05). The study included 112 patients with reactive spondyloarthritis (ReSpA) who received secukinumab (300 mg) once every two week. Following treatment at 13, 26, and 52 weeks, a significant reduction in IL-17A levels was observed in ReSpA patients, highlighting the therapeutic efficacy of secukinumab in modulating IL-17A levels. Improvements observed in both males and females were reflected in the decrease in IL-17A levels, underscoring the therapeutic impact. In both groups, the long-term efficacy of secukinumab was demonstrated through significant clinical and laboratory improvements, confirming its effectiveness in managing ReSpA. IL-17A levels in males decreased by 42%, 55%, and 68% at weeks 13, 26, and 52, respectively (p<0.001). Similarly, in females, reductions of 37%, 49%, and 60% were observed at the same time points (p<0.001). The mean baseline ASDAS score was 3.8 ± 0.7, indicating high disease activity. After 13 weeks of treatment with the IL-17A inhibitor, the mean ASDAS score decreased significantly to 2.8 ± 0.6 (p<0.001), with further reductions observed at 26 weeks (2.3 ± 0.7, p<0.001) and 52 weeks (1.9 ± 0.7, p<0.001). By week 52, 66 % of patients achieved clinically important improvement (ASDAS reduction ≥1.1), and 43% achieved major improvement (ASDAS reduction ≥2.0).
Conclusion: The progressive increase in IL-17A levels was indicative of spinal involvement being more characteristic of the urogenital form and chronic course of the disease. Secukinumab (300 mg, administered subcutaneously once every two weeks) effectively reduced IL-17A levels and improved clinical manifestations in patients with reactive spondyloarthritis (ReSpA).
REFERENCES: [1] Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview
[2] IL-17 inhibitors in axial spondyloarthritis. An overview
Acknowledgements: This abstract is part of the Internal medicine at Family medicine No2 and reflects the collaborative efforts of its members. The group has provided invaluable insights and feedback throughout the research process.
Disclosure of Interests: None declared.
© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (