Abstract

Abstract Background/Aims Pain remains a common, life-changing symptom for patients with rheumatoid (RA) and psoriatic arthritis (PsA). Its current care focuses on prescribing analgesics, particularly opioids, despite minimal supportive trial evidence and potential associated harms. Intensive management with disease-modifying anti-rheumatic drugs (DMARDs) reduces disease activity and improves function in RA and PsA. Its impacts on pain are less well established. We examined the impact of varying intensities of DMARD treatment on pain in patients with RA/PsA in a secondary analysis of three trials. Methods The trials comprised MIPA in PsA (methotrexate vs. placebo), CARDERA in early RA (triple therapy vs. monotherapy), and TITRATE in established RA (monthly assessments with DMARD uptitration and psychosocial support vs. standard care). All measured 100mm pain intensity visual analogue scores. Regression models evaluated the relationship between active vs. control treatment and: (a) achieving “low” endpoint pain scores of ≤ 34, (b) changes in pain scores between baseline and endpoint, (c) achieving ≥30% reductions in pain scores between baseline and endpoint. Results We evaluated 765 patients (from 1,023 [75%]) with endpoint pain intensity scores available. In all trials more patients achieved low endpoint pain scores (≤34) with active than control treatment (MIPA 70% vs. 42%, P=0.003; CARDERA 71% vs. 56%, P=0.011; TITRATE 67% vs. 50%; P=0.008). Multivariable models showed the associations remained significant after treatment effects were adjusted for age, sex, and baseline pain: odds ratios (ORs) 2.8 (P=0.012), 1.9 (P=0.019) and 2.1 (P=0.006) in MIPA, CARDERA, and TITRATE. The trials differed in the impact of intensive treatment on changes in pain scores. In MIPA mean changes in pain intensity scores over the trial period were similar with active and control treatment. In CARDERA (P=0.019) and TITRATE (P=0.004) mean changes in pain scores were significantly greater with active than control treatment in multivariable models (estimated differences of 6.8 and 9.4 units). The trials also differed in the impact of treatment on the proportion of patients having large reductions in pain scores (≥30). In MIPA proportionally more patients achieved this with active vs. control treatment but this was not statistically significant. In CARDERA (P=0.009) and TITRATE (P=0.002) a significantly greater proportion of patients achieved large reductions in pain scores in multivariable models with active treatment (ORs 1.9 and 2.2). Conclusion In our secondary analysis all forms of intensive management provided beneficial effects on pain in active RA and PsA. More patients achieved “low” endpoint pain scores with active treatment in all trials. In the two trials employing the most intensive management strategies (CARDERA/TITRATE) significantly greater reductions in pain scores and a greater proportion achieving substantial pain improvements with active treatment were seen. Our results support the use of intensive management to improve pain in patients with active RA/PsA. Disclosure I.C. Scott: None. D.L. Scott: None. F. Ibrahim: None.

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