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THU0171 Influence of Immunogenicity of Anti-TNF Therapy in RA Patients with a Long-Term Treatment with Infliximab or Adalimumab
  1. A. Villalba1,
  2. C. Plasencia1,
  3. D. Peiteado1,
  4. L. Nuño1,
  5. G. Bonilla1,
  6. L. Lojo1,
  7. D. Pascual2,
  8. R. del Moral2,
  9. M. T. López Casla2,
  10. A. Balsa1,
  11. E. Martin Mola1
  1. 1Dep. Rheumatology
  2. 2Dep. Immunology, Hospital Universitario La Paz, Madrid, Spain

Abstract

Background The anti-TNF therapy has been a great progress in RA patients treatment. However, a proportion of patients develop primary inefficacy or loss of response, resulting in switching or treatment discontinuation. Recent studies correlate the antidrug antibodies (ADA) development with loss of efficacy.

Objectives To asses in RA patients treated with infliximab (Ifx) or adalimumab (Ada) whether ADA development influences on the clinical efficacy and treatment duration.

Methods We studied ambispectively 174 RA patients from La Paz University Hospital who received Ifx or Ada between years 2000-2012, both in combination with synthetic DMARDs or in monotherapy. The assessment of disease activity was performed by Disease Activity Score 28 (DAS28) and clinical improvement by delta-DAS28. Measurements were performed at baseline, 1, 2 and ≥ 3 years under the biological therapy (BT). ADA and drug levels were measured by ELISA. Statistical analysis was performed using SPSS 11.0.

Results Of the 174 patients, 140 (80.5%) were women. The mean age was 57 ± 13.2 years and the disease duration was 14.7 ± 8.0 years. 128 patients (73.6%) were RF positive. The mean duration on BT was 5.0 ± 3.0 years. One hundred fifty patients (86.2%) received methotrexate, 98 other DMARDs (56.3%) and 11 (6.3%) were in monotherapy. The mean DAS28 at baseline was 5.28 ± 1.26 and there was no significant differences between DAS28 at baseline in patients with or without ADA ( 5,28±1,47 ADA+ vs 5,25±1,19 ADA-, p=0,918). Along the study, 62 patients (35.6%) developed ADA (47/105 patients (44.8%) to Ifx and 15/69 patients (21.7%) to Ada, p = 0.002). Ninety six (55.2%) patients dropped out the BT and this was more frequent in ADA positive patients [49/62 (79.0%) ADA+ vs. 47/112 (41.9%) ADA-, p <0.00001]. Most patients who discontinued by inefficacy had ADA [25/39 (64.1%) ADA+ vs 14/39 (35.9%) ADA-, p = 0.039]. Patients with ADA were more active in all studied point (at 1st year: 4.69 ± 1.15 ADA+ vs 3.43 ± 1.22 ADA-, p<0.0001; at 2nd year: 3.96 ± 1.40 ADA+ vs 3.08 ± 1.09 ADA-, p= 0.015; at 3rd year: 4.34 ± 1.26 ADA+ vs 3.21 ± 1.56 ADA-, p = 0.001). The clinical improvement was lower in ADA positive patients along this work (at 1st year: 0.94 ± 1.06 ADA+ vs 1.63 ± 1.32 ADA-, p = 0.045; at 2nd year: 0.72 ± 1,05 ADA+ vs. 1.83 ± 1.59 ADA-, p =0.021; at 3rd year: 0.44 ± 1.26 ADA+ vs 2,02 ± 1.87 ADA-, p<0.0001).

Conclusions The ADA development in RA patients treated with Ifx or Ada is correlated with a clinical inefficacy and with the therapy survival, resulting in an earlier therapy discontinuation.

Disclosure of Interest None Declared

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