Background Takayasu’s arteritis (TAK) is a large-vessel vasculitis that mainly involves the aorta and its primary branches. Glucocorticoids (GCs) are the mainstay of treatment of TAK, especially for the induction of remission. However, the majority of patients experience relapses when the dose of GCs is reduced. Many patients fail to respond to synthetic conventional immunosuppressive drugs. IL-6 and TNF-α have been shown to be involved in the pathogenesis of TAK. Biologic drugs that target IL-6 or TNF-α (TNFis) have been reported to be effective and are recommended for the treatment of TAK refractory to low-dose GC combined with conventional treatment. Recently, Th-17 cells and its related cytokines IL-17A, IL-21, and IL-23 have also been identified as involved in the pathogenesis of TAK, suggesting that targeting IL-17A might be an effective treatment for this disease.

Objectives This study aimed to investigate the efficacy of secukinumab, an anti-IL-17A monoclonal antibody, compared to treatment with TNFis for the induction of remission of patients with a relapse of TAK.

Methods This was a prospective, single center, open-label cohort study. Patients with active TAK who failed to respond to treatment with glucocorticoids combined with 2 immunosuppressive agents were treated with either secukinumab or TNFi as an add-on therapy without increase of the dosage of GCs. Complete response was defined as full resolution of signs and symptoms of active disease, normal values of inflammatory markers, no progression on imaging of involved arteries, and dose of glucocorticoid <15mg/d. Partial response was defined as the same as complete response except ESR <40mm/hour and CRP <20mg/L.

Results Nineteen patients in the secukinumab group and 34 patients in the TNFi group were enrolled. The demographic data and inflammatory markers of the two groups were comparable at baseline. The baseline dose of GC (prednisone) was ≤ 15 mg/day in all patients in both treatment groups. The combined complete and partial responses at 3 months for patients treated with secukinumab and TNFi were 31.6% and 58.8% (P =0.506) respectively, and at 6 months were 52.6% and 64.7% (P= 0.389), respectively. Similar responses to both secukinumab and TNFi we also seen for time to initiation of GCs and time to achieving a dose of prednisone ≤ 5 mg/day (Figure 1). The ESR, serum CRP, and IL-6 levels were significantly reduced compared with the baseline after 1, 3, and 6 months of treatment in both secukinumab and TNFis treatment groups. In the secukinumab treatment group 6 of 19 (31.6%) patients had their GC dosage tapered and 2 patients reduced the dose of conventional immunosuppressive agents at 6 months. In the TNFi treatment group 18 of 34 (52.9%) patients had their GC dosage tapered and 4 patients reduced the dose of conventional immunosuppressive agents at 6 months. There was no significant difference of the median dose of GC in either treatment group. No arterial structural changes were observed in patients in either the secukinumab or TNFi treatment group at 6 months. Two patients had infectious events in the secukinumab treatment group, one lead to discontinuation of the medication. Two patients in the TNFi treatment group had events leading to withdrawal from the study: one with a severe infection and one with a severe rash.

Conclusion These results suggest that secukinumab and TNFi are effective treatments for patients with TAK who fail to respond to oral GCs and conventional immunosuppressive agents, with similar response rates at 3 and 6 months.

Figure 1.

Image/graph:

REFERENCES:

NIL.

Acknowledgements: NIL.

Disclosure of Interests None Declared.

Keywords: Vasculitis

DOI: 10.1136/annrheumdis-2023-eular.3440