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We read with great interest the commentary by Rutgeerts et al1 on the value of predicting patient responses from trough serum levels of monoclonal antibodies (mAbs) against tumour necrosis factor-α (TNF). In fact, we have proposed therapeutic monitoring for rational use of anti-TNF mAb for quite some time.2
The authors point to the importance of low drug trough levels and ask how this can be explained in the absence of anti-drug antibodies (ADAs). They also pose the question whether ADAs are not always detected by routine assays. From experience with anti-TNF-treated patients with rheumatoid arthritis (RA) and Crohn's disease (CD), we can say that standard solid-phase assays (ELISAs) often fail to detect ADA because of high background values, matrix effects, for example epitope masking, and inability to detect ADA in the presence of the drug itself. Furthermore, …
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