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FRI0206 Correlation between the serum etanercept level and response to etanercept treatment in patients with rheumatoid arthritis
  1. SM Zivojinovic1,
  2. M Sefik-Bukilica2,
  3. NS Damjanov3
  1. 1Clinical IV
  2. 2Laboratory department
  3. 3Head of Institute of rheumatology, Institute of Rheumatology, Belgrade, Serbia

Abstract

Background It is well documented that the blockade of TNF-α significantly reduces disease activity in patients with rheumatoid arthritis (RA). However, at least one third of patients receiving etanercept either do not respond to treatment, or lose initial responsiveness [1]. Recent findings indicate that lack of clinical response may be related with lowering the serum drug levels.

Objectives To investigate the relationship between serum etanercept levels and response to etanercept treatment in patients with RA.

Methods The study population consisted of fifty eight patients with rheumatoid arthritis (RA), all treated with etanercept. Disease activity was assessed according to the 28-joint count Disease Activity Score (DAS28) at baseline and 6 months of therapy. Clinical response was assessed using the European League Rheumatism (EULAR) response criteria [2]. Serum etanercept levels were measured by sandwich ELISA based on the ability of etanercept to bind TNF. Antibodies against etanercept were measured by bridging ELISA (Promonitor).

Results The 47 female and 11 male were of a mean age 52.1±11.2 years (22–87) and have been living with RA for a mean of 13.2±8.2 years (2–24). At baseline the DAS28-ESR mean score was 6.1±1.0. After six months of etanercept treatment, 20 (34.5%) patients were in remission, 20 (34.5%) were in low disease activity and 18 (31%) were in moderate disease activity. The serum etanercept levels were significantly higher in patients in remission compared with patients in moderate disease activity (p=0.05). According to the EULAR response criteria, RA patients were divided into responders (52pts, 89.7%) and non-responders (6 pts, 10.3%). Median etanercept levels in all patients were 3.937mcg/ml. There were no statistical differences in etanercept levels between responders and non-responders patients (p=0.41). In addition, we stratified all patients into quartiles according to height of the etanercept level. The percentage of EULAR good responders was significantly different between the highest and the lowest quartiles (p<0.05).

Anti-etanercept antibodies were not found in any of the studied patients (0/58).

Conclusions Patients with RA who did not respond to etanercept treatment achieved lower etanercept levels compared with responding patients. Higher concentrations of the drug were associated with a better response to treatment. Further studies are needed to provide evidence for this approach.

References

  1. Morand EF, Murphy K, Mackay F, Mariette X, Marcelli C. Antidrug antibodies (ADAb) to tumour necrosis factor (TNF)-specific neutralising agents in chronic inflammatory diseases: a real issue, a clinical perspective. Ann Rheum Dis. 2013 Feb;72(2):165–78.

  2. Van Gestel AM, Anderson JJ, van Riel PL, et al. ACR and EULAR improvement criteria have comparable validity in rheumatoid arthritis trials. American College of Rheumatology European League of Associations for Rheumatology.J Rheumatol 1999; 26:705–11.

References

Disclosure of Interest None declared

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