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THU0282 Clinical efficacy to a second anti-tnf therapy is associated with the development of antibodies against the first anti-TNF therapy in patients with spondyloartrhitis
  1. S. García Carazo1,
  2. C. Plasencia1,
  3. D. Pascual Salcedo2,
  4. G. Bonilla Hernan1,
  5. L. Lojo1,
  6. A. Villalba1,
  7. L. Nuño1,
  8. L. del Olmo1,
  9. S. Gil Barato1,
  10. P. Alcocer Amores1,
  11. F. Arribas2,
  12. E. Perez3,
  13. E. Martin Mola1,
  14. A. Balsa1
  1. 1Rheumatology
  2. 2Inmunology Unit
  3. 3Biostatistic Unit, La Paz University Hospital, Madrid, Spain


Background Spondyloarthropathies (SpA) include a heterogeneous group of rheumatic diseases that mainly affect the axial skeleton and entheses. Despite the anti-TNF therapy has been demonstrated effective in SpA patients, about 30% of them develop primary or secondary inefficacy. In rheumatoid arthritis (RA) has been shown that the development of antibodies (Ab) against the first anti-TNF determines the clinical response to a second anti-TNF.

Objectives To assess if the effectiveness of second anti-TNF therapy is associated with the development of Ab against the first anti-TNF in SpA patients switching to a second anti-TNF.

Methods We studied 33 SpA patients treated with a second anti-TNF after having an inadequate response to the first anti-TNF therapy. The diagnoses were: 23 (69.7%) Ankylosing Spondylitis (AS), 6 (18.2%) undifferentiated SpA, 2 (6.1%) psoriatic SpA, 1 (3%) SpA associated with inflammatory bowel disease and 1 (3%) reactive SpA. Clinical activity was measured by ASDAS-CRP at baseline to the 1st and 2nd anti-TNF treatment and after 6 months of the switching. Clinical improvement was assessed by the Delta-ASDAS (clinically important improvement ≥1.1). Drug through levels and anti-drug Ab were measured by ELISA at the end of the fist anti-TNF treatment. Statistical analysis was performed using SPSS 11.0.

Results Our cohort included 33 patients, 18 (54.5%) male, mean age of 50.09±10 years and 21 (63.6%) HLA B27 positive. All of them were initially treated with an anti-TNF: 14 (42.4%) with infliximab (Ifx), 3 (9.1%) with adalimumab (Ada), 16 (48.5%) with etanercept (Eta). Nine out of 33 (27.3%) developed anti-drug Ab [8 anti-Ifx Ab (ATI) and 1 anti-Ada Ab (AAA)]. All patients switched to a 2nd anti-TNF, due to inefficacy: 7 (21.2%) to Ifx, 16 (48.5%) to Ada, 5 (15.2%) to Eta, 5 (15.2%) to golimumab. Clinical activity (ASDAS-CRP) was not different at baseline between first and second anti-TNF therapy (3.45±0.99 vs 3.22±0.96, p=0.24). No differences were observed between patients who developed or not anti-drug Ab at baseline to the first (3.34±0.87 with Ab vs 3.50±1.04 without Ab, p=0.93) and second (2.99±0.95 with Ab vs 3.31±0.96 without Ab, p=0.37) anti-TNF treatment. After 6 months of switching to a second anti-TNF, patients who had developed anti-drug Ab had lower clinical activity (ASDAS-CRP) than patients without anti-drug Ab (1.76±0.98 with Ab vs 2.79±1.10 without Ab, p=0.021). Moreover clinical improvement was higher in patients with anti-drug Ab (1.23±1.22 with Ab vs 0.52±1.08 without Ab, p=0.063). Most patients who had clinically important improvement had anti-drug Ab before switching [60% (6/10) vs 40% (4/10), p=0.010].

Conclusions Same as in RA, in SpA, the failure to a first anti-TNF therapy associated with the development of anti-drug Ab predicts a better clinical response to a second anti-TNF. The study of the immunogenicity in the biological treatment failure helps predict the response to a second biological treatment in SpA.

Disclosure of Interest None Declared

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