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Patients non-responding to etanercept obtain lower etanercept concentrations compared with responding patients
  1. A Jamnitski1,
  2. C L Krieckaert1,
  3. M T Nurmohamed1,3,
  4. M H Hart2,
  5. B A Dijkmans1,3,
  6. L Aarden2,
  7. A E Voskuyl3,
  8. G J Wolbink1,2
  1. 1Jan van Breemen Research Institute/Reade, Amsterdam, The Netherlands
  2. 2Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands
  3. 3VU University Medical Centre, Amsterdam, The Netherlands
  1. Correspondence to Dr G J Wolbink, Department of Rheumatology, Jan van Breemen Research Institute/ Reade, Dr Jan van Breemenstraat 2, 1056 AB Amsterdam, The Netherlands; g.wolbink{at}reade.nl

Abstract

Objective To investigate the relationship between serum etanercept levels and clinical response.

Methods In 292 etanercept-treated patients with rheumatoid arthritis clinical and pharmacological data were determined at baseline and after 1, 4 and 6 months of etanercept treatment. Differences in etanercept levels between good, moderate and European League Against Rheumatism (EULAR) non-responders were assessed after 6 months of therapy.

Results After 6 months of therapy etanercept levels were significantly higher in good responders (median (IQR) 3.78 (2.53–5.17)) compared with both moderate 3.10 (2.12–4.47) and EULAR non-responders 2.80 (1.27–3.93) (all p<0.05). There was a significant association between clinical response and serum etanercept levels (regression coefficient 0.54, 95% CI 0.21 to 0.86, p=0.001). When patients were categorised into quartiles according to the height of etanercept levels, the lowest quartile (etanercept level <2.1 mg/l) comprised 40% of all non-responders. The highest quartile (etanercept level >4.7 mg/l) comprised 35% of all good EULAR responders. Anti-etanercept antibodies were detected in none of the sera.

Conclusion The authors demonstrated that lower etanercept levels were associated with non-response. Therapeutic drug monitoring and the possibility of the adjusted dosing regimes in the selected groups of patients should be investigated further as a possible tool to optimise treatment with etanercept.

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Footnotes

  • Funding The clinical part of this study was partly financed by Pfizer (Wyeth) Pharmaceuticals. In addition, this investigation was also facilitated by the Division of Research and Education of the Jan van Breemen Research Institute/READE. The study sponsors had no involvement in the study design, in the collection, analysis and interpretation of data, in the writing of the report and in the decision to submit the paper for publication.

  • Competing interests MTN has received consultancy fees from Abbott, Roche, Pfizer, MSD, UCB, BMS and Wyeth, payment for lectures from Abbott, Roche and Pfizer and research grants from Abbott, Roche and Pfizer. BAD has received research grants from Schering-Plough, Abbott and Wyeth. GJW has received a research grant from Pfizer (Wyeth) drugs.

  • Patient consent Obtained.

  • Ethics approval The study was approved by the medical ethics committee of Reade and Slotervaart Ziekenhuis.

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

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