Abstract
248 Genome-wide association study of response to tumour necrosis factor inhibitor therapy in rheumatoid arthritis
Highlights
Electronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.Rheumatoid arthritis (RA) is a chronic autoimmune disorder affecting around 1% of the United Kingdom (UK) population [1], which leads to synovial joint inflammation and joint damage
There are a number of Tumour necrosis factor (TNF) inhibitor (TNFi) biologics and biosimilars licensed for treatment of RA within the UK: Infliximab (Remicade, biosimilars: Remsima and Inflectra), adalimumab (Humira), certolizumab pegol (Cimzia), and golimumab (Simponi) are antibodies or fragments of antibodies that are targeted towards the TNF, whilst etanercept (Enbrel, biosimilar: Benapali) comprises two TNFR2 extracellular domains fused to the IgG1 Fc
In a large study of TNFi response in the UK, we have found no variants predictive of change in Disease Activity Score 28 (DAS28) score over the first 3–6 months of treatment
Summary
Given the expense of these drugs (around 5000–10,000 GBP per patient per year in the UK) and the potential for detriment to non-responding patients, the identification of predictors of response from pre-treatment (baseline) characteristics would be of great clinical, societal and economic benefit. The importance of this question motivated the formation of the UK MAximizing Therapeutic Utility in RA (MATURA) consortium [5], which has the wider remit of using blood-based biomarkers and synovial pathobiology to inform the stratification of all stages of RA treatment
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