Effect of initiating biologics compared to intensifying conventional DMARDs on clinical and MRI outcomes in established rheumatoid arthritis patients in clinical remission: Secondary analyses of the IMAGINE-RA trial
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Objectives: To compare the effect of treat-to-target-based escalations in conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and biologics on clinical disease activity and magnetic resonance imaging (MRI) inflammation in a rheumatoid arthritis (RA) cohort in clinical remission. Method: One-hundred patients with established RA, Disease Activity Score based on 28-joint count–C-reactive protein (DAS28-CRP) < 3.2, and no swollen joints (hereafter referred to as ‘in clinical remission’) who received csDMARDs underwent clinical evaluation and MRI of the wrist and second to fifth metacarpophalangeal joints every 4 months. They followed a 2 year MRI treatment strategy targeting DAS28-CRP ≤ 3.2, no swollen joints, and absence of MRI osteitis, with predefined algorithmic treatment escalation: first: increase in csDMARDs; second: adding a biologic; third: switch biologic. MRI osteitis and Health Assessment Questionnaire (HAQ) (co-primary outcomes) and MRI combined inflammation and Simplified Disease Activity Index (SDAI) (key secondary outcomes) were assessed 4 months after treatment change and expressed as estimates of group differences. Statistical analyses were based on the intention-to-treat population analysed using repeated-measures mixed models. Escalation to first biologic compared to csDMARD escalation more effectively reduced MRI osteitis (difference between least squares means 1.8, 95% confidence interval 1.0–2.6), HAQ score (0.08, 0.03–0.1), MRI combined inflammation (2.5, 0.9–4.1), and SDAI scores (2.7, 1.9–3.5). Treat-to-target-based treatment escalations to biologics compared to escalation in csDMARDs more effectively improved MRI inflammation, physical function, and clinical disease activity in patients with established RA in clinical remission. Treatment escalation in RA patients in clinical remission reduces clinical and MRI-assessed disease activity. Trial registration: Clinicaltrials.gov identifier: NCT01656278.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Scandinavian Journal of Rheumatology |
| Vol/bind | 51 |
| Udgave nummer | 4 |
| Sider (fra-til) | 268-278 |
| ISSN | 0300-9742 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
S Møller-Bisgaard reports grants and non-financial support from AbbVie, during the conduct of the study. ML Hetland reports grants from AbbVie, grants and personal fees from Biogen, grants from BMS, personal fees from Celltrion, grants from Eli Lilly Danmark A/S, personal fees from Janssen Biologics BV, grants from Lundbeck Fonden, personal fees from MSD, grants and personal fees from Pfizer, grants from Roche, personal fees from Samsung Biopis, grants from Sandoz, and grants from Novartis, outside the submitted work; and Dr Hetland chairs the steering committee of the Danish Rheumatology Quality Registry (DANBIO), which receives public funding from the hospital owners and funding from pharmaceutical companies. ML Hetland co-chairs EuroSpA, which generates real-world evidence of treatment of psoriatic arthritis and axial spondyloarthritis based on secondary data, and is partly funded by Novartis. R Christensen reports Lecture: Research Methods (Pfizer, DK; 2017), Lecture: GRADE, Lecture (Celgene, DK; 2017), Ad Board Lecture: CAM (Orkla Health, DK; 2017), Project Grant: ‘GreenWhistle’ (Mundipharma, 2019), Lecture: Diet in RMD (Novartis, DK; 2019), Consultancy Report: Network MA’s (Biogen, DK; 2017), Ad Board Lecture: GRADE (Lilly, DK; 2017), Consultancy Report: GRADE (Celgene, 2018), and Lecture: Network MA’s (LEO; 2020), all outside the submitted work; and Musculoskeletal Statistics Unit, The Parker Institute is grateful for the financial support received from public and private foundations, companies, and private individuals over the years. The Parker Institute is supported by a core grant from the Oak Foundation; The Oak Foundation is a group of philanthropic organizations that, since its establishment in 1983, has given grants to not-for-profit organizations around the world. LM Ørnbjerg reports grants from AbbVie during the conduct of the study. M Boesen reports grants from AbbVie during the conduct of the study; personal fees from AbbVie, personal fees from UCB, personal fees from Eli Lilly, grants and personal fees from Image Analysis Group, and grants from Esaote, outside the submitted work. M Østergaard reports grants from AbbVie, during the conduct of the study; grants, personal fees, and non-financial support from AbbVie, grants, personal fees, and non-financial support from BMS, personal fees from Boehringer-Ingelheim, personal fees from Eli Lilly, personal fees and non-financial support from Janssen, grants, personal fees, and non-financial support from Merck, personal fees and non-financial support from Pfizer, personal fees and non-financial support from Roche, grants, personal fees, and non-financial support from UCB, grants and personal fees from Celgene, personal fees from Sanofi, personal fees from Regeneron, and grants, personal fees, and non-financial support from Novartis outside the submitted work. No other disclosures relevant to this article were reported.
Publisher Copyright:
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