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Annals of the Rheumatic Diseases 2009;68:1787-1788; doi:10.1136/ard.2009.109702
Copyright © 2009 BMJ Publishing Group Ltd & European League Against Rheumatism.

LETTER

Decreased clinical response to adalimumab in ankylosing spondylitis is associated with antibody formation

M K de Vries1, E Brouwer5, I E van der Horst-Bruinsma1, A Spoorenberg6, J C van Denderen3, A Jamnitski3, M T Nurmohamed1,3, B A C Dijkmans1,3, L A Aarden2,4, G J Wolbink2,3

1 VU University Medical Centre, Amsterdam, The Netherlands
2 Sanquin Research, Amsterdam, The Netherlands
3 Jan van Breemen Institute, Amsterdam, The Netherlands
4 Landsteiner Laboratory Academic Medical Centre, Amsterdam, The Netherlands
5 University Medical Center, Groningen, The Netherlands
6 Medical Center, Leeuwarden, The Netherlands

Correspondence to:
Correspondence to Dr I E van der Horst-Bruinsma, VU University Medical Centre, Rheumatology Department, room 3A-64, P O Box 7057, 1007 MB Amsterdam, The Netherlands; ie.vanderhorst@vumc.nl

Accepted 7 February 2009

The first 150 words of the full text of this article appear below.

Treatment with anti-tumour necrosis factor (TNF) is very effective in most patients with ankylosing spondylitis (AS), but inefficacy occurs in about 40% of cases.1 Antibody formation against TNF blocking agents is an increasingly recognised problem;2 however, no data have yet been reported on antibody formation against adalimumab (anti-adalimumab) in AS. Lack of response can be explained in two ways: (1) TNF might not be important for disease activity in certain patients; and (2) TNF inhibition might be insufficient. The latter could be caused by excessive production of TNF, low compliance of the patient, insufficient dosing or an enhanced clearance of adalimumab due to antibody formation. Adalimumab is a fully human monoclonal antibody against TNF but, despite this fact, an immune response still can be provoked by the antigen binding site also known as the idiotype. In previous studies we have described the problem of immunogenicity of TNF blocking drugs in . . . [Full text of this article]


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