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Rheumatology Advance Access originally published online on April 4, 2007
Rheumatology 2007 46(6):1034-1035; doi:10.1093/rheumatology/kem041
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

LETTERS TO THE EDITOR

Combined tumour necrosis factor-{alpha} and tumour necrosis factor receptor genotypes could predict rheumatoid arthritis patients’ response to anti-TNF-{alpha} therapy and explain controversies of studies based on a single polymorphism

A. Chatzikyriakidou, I. Georgiou, P. V. Voulgari1, A. I. Venetsanopoulou1 and A. A. Drosos1

Genetics Unit, Department of Obstetrics and Gynaecology, and 1Rheumatology Clinic, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece

Correspondence to: Prof. A. A. Drosos Rheumatology Clinic, Department of Internal Medicine, Medical School, University of Ioannina, 45110 Ioannina, Greece. E-mail: adrosos@cc.uoi.gr

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SIR, Tumour necrosis factor-{alpha} (TNF-{alpha}) blocker therapies are widely used in the treatment of chronic inflammatory diseases. However, patients show large heterogeneity in their response to anti-TNF-{alpha} therapy. The genotypic background of TNF-{alpha} and TNF receptor (TNFR) genes could account for patients’ resistance to TNF-{alpha} blockers [1, 2]. HLA-DR haplotypes have been related with rheumatoid arthritis (RA) susceptibility, severity and course [3], but TNF and TNFR polymorphisms seem to have independent predictive value of patients’ response to anti-TNF-{alpha} therapy [2, 4, 5. . . [Full Text of this Article]


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