FRI0019 MRI INFLAMMATION, DISEASE ACTIVITY AND FUNCTIONAL IMPAIRMENT ARE MORE EFFECTIVELY REDUCED BY ESCALATION TO BIOLOGICS COMPARED TO CSDMARD-ESCALATION IN RHEUMATOID ARTHRITIS PATIENTS IN CLINICAL REMISSION FOLLOWING A TREAT-TO-TARGET STRATEGY: SECONDARY ANALYSES OF THE IMAGINE-RA TRIAL
Authors: S. Møller-Bisgaard, K. Hørslev-Petersen, B. Ejbjerg, M. L. Hetland, R. Christensen, L. Ørnbjerg, D. Glinatsi, J. Møllenbach Møller, M. Boesen, K. Stengaard-Pedersen, O. Rintek Madsen, B. Jensen, J. Villadsen, E. M. Hauge, P. Bennett, O. Hendricks, K. Asmussen, M. Kowalski, H. M. Lindegaard, H. Bliddal, N. Steen Krogh, T. Ellingsen, A. Nielsen, A. G. Jurik, L. Balding, H. Thomsen, M. Ǿstergaard
Journal: Annals of the Rheumatic Diseases (2020)

Background: The effect of different treatment escalations on MRI inflammation in rheumatoid arthritis (RA) patients following an MRI treat-to-target (T2T) strategy has not previously been investigated. Objectives: To compare the effect of different treatment escalations on MRI inflammation, physical function and disease activity in RA patients in clinical remission, following an MRI T2T strategy. Methods: One hundred RA patients in clinical remission (DAS28-CRP&lt;3.2 and no swollen joints), on conventional synthetic (cs) DMARDs following an MRI T2T strategy targeting DAS28-CRP≤3.2, no swollen joints plus absence of MRI osteitis, were followed for 2 years with clinical and MRI (wrist and 2 nd -5 th MCP joints) evaluation every 4 months 1 . If target was not met, a predefined treatment escalation algorithm dictated: First: increase in csDMARDs (A), second: adding a TNF inhibitor (TNFi) (B), third and onwards: switch between biologics (C). If target was met, no change in baseline csDMARDs was done (D). Outcomes were assessed 4 months after treatment change. MRIs were evaluated with known chronology by one experienced reader. Repeated measures mixed linear models were used to express estimates of group differences on predefined co-primary outcomes (MRI osteitis, HAQ) and key secondary outcomes (MRI combined inflammation, Simplified Disease Activity Index (SDAI)). Results: Escalation to first TNFi (B) or to 2 nd or later biologic (C) compared to csDMARDs (A) was consistently more effective on all outcomes (e.g. in group B osteitis was reduced with 1.8 units more than A) (Table). Unchanged (D) compared to escalation in csDMARD (A) treatment did not differ, except for HAQ-score. Escalation to a 2 nd or later biologics (C) compared to the first TNFi (B) was more effective suppressing MRI inflammation. Escalation to TNFi treatment (B) or to 2 nd or later biologic (C) compared to unchanged treatment (D) was more effective on all outcomes except from HAQ-score (no difference between groups). Comparisons of treatment escalations 1 A: Increment in csDMARD mono/combination therapy (n=73)); B: Switch from csDMARD combination therapy to TNFi (n=39); C: Switch from TNFi to 2 nd biologic/switch between biologics (n=21); D: No change in csDMARDs from baseline (n=58) A vs B A vs C A vs D B vs C B vs D C vs D Outcomes Primary MRI Osteitis 1.8 (1.0; 2.6) p&lt;.0001 3.6 (2.3; 4.8) p&lt;.0001 0.3 (−0.3; 1.0) p=.32 1.8 (0.8; 2.9) p=.0006 −1.4 (−2.4; −0.5) p=.0045 −3.3 (−4.6; −1.9) p&lt;.0001 HAQ 0.081 (0.033; 0.13) p=.0011 0.091 (0.031; 0.15) p=.0032 0.054 (0.014; 0.095) p=.0091 0.0092 (−0.051; 0.070) p=.77 −0.027 (−0.082; 0.028) p=.33 −0.037 (−0.10; 0.031) p=.29 Key secondary MRI combined inflammation a 2.5 (0.9; 4.1) p=.0018 5.4 (3.1; 7.7) p&lt;.0001 0.4 (−0.9; 1.8) p=.52 2.9 (0.8; 4.9) p=.0064 −2.1 (−4.0; −0.2) p=.032 −5.0 (−7.5; −2.4) p=.0002 SDAI 2.7 (1.9; 3.5) p&lt;.0001 2.4 (1.4; 3.4) p&lt;.0001 0.5 (−0.2; 1.2) p=.14 −0.3 (−1.3; 0.7) p=.60 −2.2 (−3.1; −1.3) p&lt;.0001 −1.9 (−3.0; 0.8) p=.0006 1 Estimates of group differences (least squares means (95% CI)). a Sum score of synovitis, osteitis and tenosynovitis Conclusion: T2T-based treatment escalations to biologics compared to csDMARD-escalations more effectively improved MRI inflammation, physical function and disease activity. Further optimization of the treatment in RA patients in clinical remission may improve long-term outcomes. References: [1]Møller-Bisgaard et al. JAMA 2019 Disclosure of Interests: Signe Møller-Bisgaard Grant/research support from: AbbVie, Consultant of: BMS, Speakers bureau: BMS, Celgene, Pfizer, Kim Hørslev-Petersen: None declared, Bo Ejbjerg: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Robin Christensen: None declared, Lykke Ørnbjerg: None declared, Daniel Glinatsi: None declared, Jakob Møllenbach Møller: None declared, Mikael Boesen Consultant of: AbbVie, AstraZeneca, Eli Lilly, Esaote, Glenmark, Novartis, Pfizer, UCB, Paid instructor for: IAG, Image Analysis Group, AbbVie, Eli Lilly, AstraZeneca, esaote, Glenmark, Novartis, Pfizer, UCB (scientific advisor)., Speakers bureau: Eli Lilly, Esaote, Novartis, Pfizer, UCB, Kristian Stengaard-Pedersen: None declared, Ole Rintek Madsen: None declared, Bente Jensen: None declared, Jan Villadsen: None declared, Ellen Margrethe Hauge: None declared, Philip Bennett: None declared, Oliver Hendricks: None declared, Karsten Asmussen: None declared, Marcin Kowalski: None declared, Hanne Merete Lindegaard: None declared, Henning Bliddal Grant/research support from: received research grant fra NOVO Nordic, Consultant of: consultant fee fra NOVO Nordic, Niels Steen Krogh: None declared, Torkell Ellingsen: None declared, Agnete Nielsen: None declared, Anne Grethe Jurik: None declared, Lone Balding: None declared, Henrik Thomsen: None declared, Mikkel Ǿstergaard Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Merck, and Novartis, Consultant of: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB