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Rheumatology Advance Access originally published online on April 26, 2005
Rheumatology 2005 44(6):705-707; doi:10.1093/rheumatology/keh662
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

EDITORIAL

The response to anti-TNF-{alpha} treatment: gene regulation at the bedside

N. de Vries and P. P. Tak

Division of Clinical Immunology and Rheumatology, AMC/University of Amsterdam, Amsterdam, The Netherlands.

Correspondence to: N. de Vries, Division of Clinical Immunology and Rheumatology, AMC/University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail: Niek.deVries@amc.uva.nl

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

Approximately 40% of the patients with rheumatoid arthritis do not fulfil the ACR20 response criteria 3 months after initiation of any of the current therapies targeting tumour necrosis factor {alpha} (TNF-{alpha}) [1–3]. These patients are not only exposed to an expensive treatment strategy but they also risk serious side-effects, notably the increased risk of tuberculosis. It would clearly be useful if we could identify those patients who are not likely to respond satisfactorily to these therapies or who are likely to develop side-effects.

Scientific progress in recent years has offered the promise that indeed such drug effects might be predicted. The elucidation of the complete human genome sequence, the efforts to describe genetic variation in large databases and the introduction of high-throughput screening techniques for genetic polymorphisms have stimulated the development of pharmacogenetic research on drug responses. Clearly, the anti-TNF-{alpha} field, characterized by expensive drugs, strong variability in . . . [Full Text of this Article]


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