Objective To assess safety and efficacy of TNF-α antagonists and tocilizumab in patients with Takayasu arteritis (TAK). Methods and Results Two-hundred nine patients with TAK [median age of 29 years [7–62], and 186 (89%) females] were included. They received either TNF-α antagonists [n = 132 (63%) with 172 lines; infliximab (n = 109), adalimumab (n = 45), golimumab (n = 8), certolizumab (n = 6) and etanercept (n = 5)], or tocilizumab [n = 77 (37%) with 121 lines; intravenous and subcutaneous in 95 and 26 cases, respectively]. A complete response at 6 months was evidenced in 101/152 (66%) on TNF-α antagonists and 75/107 (70%) on tocilizumab, respectively. Age ≥ 30 years [OR = 2.09 [1.09; 3.99]] was associated with complete response, whereas vascular signs [0.26 [0.1; 0.65]], baseline prednisone ≥ 20 mg/day [0.51 [0.28; 0.93]] were negatively associated with the complete response to TNF-α antagonists or tocilizumab. During a median follow-up of 36 months, 103 relapses were noted. Supra-aortic branches and thoracic aorta involvements [HR 2.44 (1.06; 5.65) and 3.66 (1.18; 11.4), respectively], and systemic signs at baseline [HR 2.01 (1.30; 3.11)] were significantly associated with relapse. The cumulative incidence of treatment discontinuation and relapse were similar in TNFα antagonists and tocilizumab. Fifty-eight (20%) adverse effects occurred on biological-targeted therapies of whom 37 (21%) and 21 (17%), (p= 0.4) on TNF-α antagonists and tocilizumab, respectively. Conclusion This large multicentre study shows high efficacy of biological-targeted treatments in refractory TAK. Efficacy, relapse and drug retention rate were equivalent with TNF-α antagonists and tocilizumab.

The objective of this study was to report the long-term use of tumor necrosis factor (TNF) inhibitors in case series of patients with Takayasu's arteritis refractory to standard immunosuppressive treatment. Nine women (median age of 29 years) with refractory Takayasu's arteritis were treated with TNF inhibitors. Prior to TNF inhibitor administration, all patients received standard immunosuppressive treatment for 16 to 112 months including steroids and immunomodulators. All but one patient presented with high activity of disease (median ESR 80 mm/h, C-reactive protein level 16.8 mg/l, interleukin-6 level 7.2 pg/ml) that was confirmed with positron emission tomography (PET) with (18)F-deoxyglucose. Eight patients were treated with infliximab and one was treated with adalimumab, respectively. The median duration of treatment was 36 months (12 to 84 months). For induction treatment, we used infliximab 200-300 mg every 4-6 weeks and adalimumab 40 mg every 2 weeks. The treatment resulted in complete remission in five (55.6%) patients and incomplete remission in three (33.3%) patients. We were able to taper the dose of prednisone to ≤10 mg daily in all patients. Median levels of ESR, C-reactive protein, and interleukin-6 diminished to 20 mm/h, 1.0 mg/l, and 1.0 pg/ml, respectively. Repeated PET showed lower activity of vasculitis in six (85.7%) of seven patients. The treatment was safe and well-tolerated. Only one patient developed allergic reactions after infusions of infliximab. Four patients developed relapse of vasculitis when we tried to increase the dosing interval of infliximab to 6-8 weeks. TNF inhibitors were highly effective and safe in patients with refractory Takayasu's arteritis.

Our case series suggests that CZP may be an effective and steroid-sparing treatment option in patients with active TA even if they did not previously respond to other TNF inhibitors or tocilizumab.

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