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The timing of serum infliximab loss, or the appearance of antibodies to infliximab (ATI), is related with the clinical activity in ATI-positive patients with rheumatoid arthritis treated with infliximab
  1. Ch Plasencia1,
  2. D Pascual-Salcedo2,
  3. P Alcocer1,
  4. M G Bonilla1,
  5. A Villalba1,
  6. D Peiteado1,
  7. F Arribas2,
  8. J Díez3,
  9. M T Lopez-Casla2,
  10. E Martín-Mola1,
  11. A Balsa1
  1. 1 Rheumatology Department, La Paz University Hospital-Idipaz, Madrid, Spain
  2. 2 Immunology Unit, La Paz University Hospital-Idipaz, Madrid, Spain
  3. 3 Statistics Department, La Paz University Hospital-Idipaz, Madrid, Spain
  1. Correspondence to Dr Chamaida Plasencia, Rheumatology Department, La Paz University Hospital-Idipaz, Paseo la Castellana 261, Madrid PC 28046, Spain; chamiplasencia{at}

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In patients with rheumatoid arthritis (RA), the development of antibodies to infliximab (ATI) is associated with poor clinical response.1 ,2–7 Nevertheless, there is no plausible explanation for why not all patients with ATI experience high disease activity. To investigate whether the timing of ATI appearance and/or drug disappearance is correlated with clinical activity, we measured the infliximab (Ifx) and ATI levels in patients 4 weeks after infusion (n+4).

Eleven ATI-positive patients with RA receiving Ifx every 8 weeks were included. Disease activity was assessed by DAS28 and European League Against Rheumatism (EULAR) criteria at baseline, and during weeks n and n+8. The serum drug and ATI levels were determined using a capture and bridging ELISA, as previously described,1 ,6 ,8–10 at weeks n, n+4 and n+8.

Patients were divided according to the findings from week n+4: Group 1 (ATI-positive=without Ifx and ATI-positive, ATI-negative=with or without Ifx and ATI-negative); Group 2 (with Ifx=ATI-negative and with Ifx, without Ifx=ATI-positive or ATI-negative and without Ifx). Table 1 shows the patients’ demographic and clinical characteristics. At week n+8, four patients were moderate responders and …

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  • Contributors ChP, DP-S, EM-M and AB have written this article. DP-S, PA, MTL-C and ChP have carried out the data collection and databases. AV, DP, MGB, PA, AB and ChP have done the clinical evaluation of patients. JD and ChP have done the statistical analysis. DP-S and FA have performed the laboratory assays.

  • Funding This study was supported by unrestricted grants from Pfizer, and the RETICS Program, RD08/0075 (RIER) from ‘Instituto de Salud Carlos III’ (ISCIII).

  • Competing interests AB has received fees from Roche, Schering-Plough, Wyeth, Abbott, BMS and USB. E.M-M. is a consultant and a member of the Pfizer speakers’ bureaus, MSD, UCB and Abbott. ChP, DP-S, MGB and DP have received speaker honoraria from Pfizer. All other authors have declared no conflicts of interest.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.