title: The immunogenicity to the first anti-TNF therapy determines the outcome of switching to a second anti-TNF therapy in spondyloarthritis patients.
abstract: BACKGROUND
  Anti-TNF drugs have proven to be effective against spondyloarthritis (SpA), although 30% of patients fail to respond or experience adverse events leading to treatment discontinuation. In rheumatoid arthritis, the presence of anti-drug antibodies (ADA) against the first TNF inhibitor influences the outcome after switching. Our aim was to assess whether the response to a second anti-TNF drug is related to the previous development of ADA to the first anti-TNF drug SpA patients.
  
  
  METHODS
  Forty-two SpA patients began a second anti-TNF drug after failing to respond to the first anti-TNF therapy. Clinical activity was assessed by the Ankylosing Spondylitis Disease Activity Score (ASDAS) at baseline (at the beginning of the first and second anti-TNF therapy) and at 6 months after switching. The drug and ADA levels were measured by ELISA before each administration.
  
  
  RESULTS
  All patients were treated with anti-TNF drugs and mainly due to inefficacy were switched to a second anti-TNF drug. Eleven of 42 (26.2%) developed ADA during the first biologic treatment. At baseline, no differences in ASDAS were found in patients with or without ADA to the first anti-TNF drug (3.52 ± 1.03 without ADA vs. 3.14 ± 0.95 with ADA, p = 0.399) and to the second anti-TNF drug (3.36 ± 0.94 without ADA vs. 3.09 ± 0.91 with ADA, p = 0.466). At 6 months after switching, patients with previous ADA had lower disease activity (1.62 ± 0.93 with ADA vs. 2.79 ± 1.01 without ADA, p = 0.002) and most patients without ADA had high disease activity state by the ASDAS (25 out of 31 (80.6%) without ADA vs. 3 out of 11 (27.3%) with ADA, p = 0.002).
  
  
  CONCLUSIONS
  In SpA the failure to respond to the first anti-TNF drug due to the presence of ADA predicts a better clinical response to a second anti-TNF drug.
authors.forename: Chamaida
authors.initials: C
authors.lastname: Plasencia
authors.forename: Dora
authors.initials: D
authors.lastname: Pascual-Salcedo
authors.forename: Sara
authors.initials: S
authors.lastname: García-Carazo
authors.forename: Leticia
authors.initials: L
authors.lastname: Lojo
authors.forename: Laura
authors.initials: L
authors.lastname: Nuño
authors.forename: Alejandro
authors.initials: A
authors.lastname: Villalba
authors.forename: Diana
authors.initials: D
authors.lastname: Peiteado
authors.forename: Florencia
authors.initials: F
authors.lastname: Arribas
authors.forename: Jesus
authors.initials: J
authors.lastname: Díez
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: López-Casla
authors.forename: Emilio
authors.initials: E
authors.lastname: Martín-Mola
authors.forename: Alejandro
authors.initials: A
authors.lastname: Balsa
mesh_terms: D000328:Adult; D000906:Antibodies / Q000097:blood*; D018501:Antirheumatic Agents / Q000276:immunology* / Q000627:therapeutic use*; D057915:Drug Substitution; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D025241:Spondylarthritis / Q000097:blood / Q000188:drug therapy*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000906:Antibodies; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha
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