Background Pain is a major problem in RA, but is not fully explained by inflammation.
Objectives We investigated factors predicting bodily pain 1 year after initiation of anti-TNF or conventional DMARD therapy change in British Society for Rheumatology Biologics Register (BSRBR) participants with RA, and baseline patient-reported factors that predicted discontinuation of TNFα-inhibitors.
Methods Data were retrieved from BSRBR-RA databases for baseline and up to 1 year after commencing TNFα-inhibitors (n=11995) or non-biologic DMARDs (n=3632). Norm-based SF36-Bodily Pain scores were used. DAS28-P was derived as the proportion of 28 joint disease activity score attributed to patient-reported factors. Adjusted odds ratios (aOR) using logistic regressions were calculated.
Results Pain was severe at baseline (medians 25, 30) and incompletely improved during follow up (medians 34, 34 respectively) in TNF-inhibitor and control cohorts. Baseline pain was associated with DAS28-P, worse function, worse mental health, and higher DAS28. After logistic regression, independent significant predictors of worse than median pain at follow up after commencing either TNF-inhibitor or non-biologic DMARD were baseline pain, DAS28-P, worse function, worse mental health and co-morbidities. Older age, male gender, smoking and high BMI were additional predictors of worse pain outcomes in participants who received TNFα-inhibitors (Table 1). Some DMARDs were associated with better pain.
Baseline pain predicted discontinuation of TNFα-inhibitors within the first year (aOR 1.13 (95% CI 1.05–1.22)); as did smoking (1.20 (1.06–1.36)), worse function (1.17 (1.08–1.26)), and systemic manifestations (1.15 (1.02–1.28)).
Conclusions Pain may improve but remains a problem for people with treated RA. Worse pain outcomes are predicted by factors different to those typically used to predict inflammatory disease activity. Pain predicts treatment failure with TNFα-inhibitors. Improved pain management should complement inflammatory disease suppression in RA.
Acknowledgements Funding: Pfizer Ltd.
We would like to acknowledge the BSR Biologics Register for the collection, provision and preparation of the data used for this study.
Disclosure of Interest D. Mcwilliams Grant/research support: Pfizer Ltd, D. Walsh Grant/research support: Pfizer Ltd