Background/Purpose: Spondyloarthropathies (SpAs) encompass a heterogeneous group of diseases that primarily affect the axial skeleton and entheses. Although anti-TNF drugs have proven to be effective against SpA, approximately 30% of patients fail to respond or experience adverse events leading to treatment discontinuation. In rheumatoid arthritis, it has been shown that the development of antibodies (Abs) against the first anti-TNF treatment determines the response to the second anti-TNF treatment. Our aim was to assess whether the response to a second anti-TNF treatment after failing to respond to a first TNF antagonist is related to the previous development of Abs to the first TNF inhibitor.

Methods: We studied 33 patients diagnosed with SpA who began treatment with a second anti-TNF after failing to respond to the first anti-TNF: 23 (69.7%) patients with ankylosing spondylitis (AS), 6 (18.3%) with undifferentiated SpA, 3 (9%) with psoriatic SpA and 1 (3%) with SpA secondary to reactive arthritis. Clinical activity was assessed by the Ankylosing Spondylitis Disease Activity Score (ASDAS) at baseline (at the beginning of the 1º and 2º anti-TNF treatments) and at 6 months after switching. Clinical improvement was evaluated using the delta-ASDAS. The drug and anti-drug Ab (ADA) levels were measured by ELISA before each administration.

Results: Of the 33 patients examined, 18 (54.5%) were male. The mean age was 50.1±10.2 years, and 75% (21/28) were positive for HLA B27. All patients were initially treated with anti-TNF drugs; 14/33 (42.4%) were treated with infliximab (Ifx), 3/33 (9.1%) with adalimumab (Ada) and 16/33 (48.5%) with etanercept (Eta). Nine of 33 (27.3%) developed ADAs during the first biologic treatment [8 Abs to Ifx (ATI) and 1 Abs to Ada (ATA)]. Mainly due to inefficacy, the first anti-TNF was exchanged for a second anti-TNF: 7 (21.2%) switched to Ifx, 16 (48.5%) to Ada, 5 (15.2%) to Eta and 5 (15.1%) to golimumab (Gol). No differences in ASDAS were not observed at baseline in patients with or without ADAs to the first (3.35±0.87 with ADAs vs 3.51±1.04 without ADAs, p=0.953) and second (2.99±0.96 with ADAs vs 3.31±0.97 without ADAs, p=0.392) anti-TNF treatments.At six months after switching, patients who had previously developed ADAs had lower disease activity (1.76±0.98 with ADAs vs 2.79±1.11 without ADAs, p=0.020), and a trend was observed towards greater clinical improvement (delta-ASDAS 1.23±1.22 with ADAs vs 0.52±1.08 without ADAs, p=0.065). At six months after switching, most patients without ADAs were classified as having high or very high disease activity state by the ASDAS (18 out of 24 (75%) without ADAs vs 3 out of 9 (33.3%) with ADAs, p=0.022), and more patients with ADAs had inactive disease (2 out of 9 (22.2%) with ADAs vs 1 out of 24 (4.2%) without ADAs, p=0.022).

Conclusion: In SpA, the failure to respond to the first anti-TNF treatment due to the development of ADAs predicts a better clinical response to a second anti-TNF treatment. The study of immunogenicity in biological treatment failure may help predict the response to a second biological treatment for SpA.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-immunogenicity-to-the-first-anti-tnf-therapy-determines-the-outcome-of-switching-to-a-second-anti-tnf-in-spondyloarthritis-patients/