4.7 Article

Disproportionate articular pain is a frequent phenomenon in rheumatoid arthritis and responds to treatment with sarilumab

Journal

RHEUMATOLOGY
Volume 62, Issue 7, Pages 2386-2393

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keac659

Keywords

RA; IL-6; sarilumab; pain; analgesia

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This study assessed the effects of IL-6 inhibitor sarilumab on disproportionate articular pain (DP) in patients with rheumatoid arthritis (RA). The results showed that about one-quarter of RA patients experienced DP and sarilumab treatment had a positive effect on DP.
Objectives In some patients with RA, joint pain is more severe than expected based on the amount of joint swelling [referred to as disproportionate articular pain (DP)]. We assessed DP prevalence and the effects of sarilumab, an IL-6 inhibitor, on DP. Methods Data from RA patients treated with placebo or 200 mg sarilumab in the phase 3 randomized controlled trials (RCTs) MOBILITY and TARGET, adalimumab 40 mg or sarilumab 200 mg in the phase 3 RCT MONARCH and sarilumab 200 mg in open-label extensions (OLEs) were used. DP was defined as an excess tender 28-joint count (TJC28) over swollen 28-joint count (SJC28) of >= 7 (TJC28 - SJC28 >= 7). Treatment response and disease activity were determined for patients with and without DP. Results Of 1531 sarilumab 200 mg patients from RCTs, 353 (23%) had baseline DP. On average, patients with DP had higher 28-joint DAS using CRP (DAS28-CRP) and pain scores than patients without DP, whereas CRP levels were similar. After 12 and 24 weeks, patients with baseline DP treated with sarilumab were more likely to be DP-free than those treated with placebo or adalimumab. In RCTs, more sarilumab-treated patients achieved low disease activity vs comparators, regardless of baseline DP status. In OLEs, patients were more likely to lose rather than gain DP status. Conclusion About one-quarter of patients with RA experienced DP, which responded well to sarilumab. These data support the concept that other mechanisms (potentially mediated via IL-6) in addition to inflammation may contribute to DP in RA.

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