OP0134 ULTRASOUND IN THE MANAGEMENT OF EARLY RHEUMATOID ARTHRITIS: MRI OUTCOME DATA FROM THE ARCTIC RANDOMIZED CONTROLLED STRATEGY TRIAL
Authors: Ulf Sundin, Anna-Birgitte Aga, Øivind Skare, Lena B Norberg, Till Uhlig, Hilde Berner Hammer, Désirée van der Heijde, Tore K. Kvien, Siri Lillegraven, Espen Haavardsholm
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> It has been debated whether treatment outcomes in early RA would be improved by targeting imaging remission, assessed by ultrasound or MRI, in addition to clinical remission. The primary analyses of the ARCTIC and TaSER trials (1, 2) did not show a beneficial effect of adding structured ultrasound assessment to a treat-to-target tight control strategy. However, both studies reported a trend toward less radiographic progression in the ultrasound arm. <h3>Objectives</h3> We aimed to investigate whether management of early RA by a tight control strategy incorporating ultrasound information in treatment decision-making would lead to improvement in MRI inflammation or less structural damage, compared to a conventional tight control strategy. <h3>Methods</h3> The ARCTIC trial was a 24-month RCT with inclusion criteria age 18-75 years, fulfillment of ACR/EULAR criteria for RA, DMARD-naivety, &lt; 2 years from first patient reported swollen joint, and indication for DMARD treatment. Patients were randomized to an ultrasound tight control strategy targeting DAS &lt; 1.6, no swollen joints and no power-Doppler signal in any joint, or a conventional strategy targeting DAS &lt; 1.6 and no swollen joints. Patients in both arms were treated by the same treat-to-target drug escalation algorithm starting with MTX, then triple combination therapy MTX/SSZ/HCQ, then biologic DMARD. In the ultrasound arm, treatment was stepped up if indicated by the ultrasound score, overruling the DAS and swollen joint count. MRI of dominant wrist and hand was performed at 6 times and scored in chronological order by a reader blinded to study arm and clinical data. MRI acquisitions and scoring were done according to the RAMRIS (3) recommendations. Of the 230 patients in ARCTIC, 218 (ultrasound n=116, conventional n=102) had MRI at baseline and ≥ 1 follow-up visit, and were included in the analyses. RAMRIS synovitis, tenosynovitis and bone marrow edema scores were summarized to a combined inflammation score; scores for erosions and joint space narrowing to a combined damage score. Mean change from baseline to each follow-up was estimated by a linear mixed model adjusted for baseline score, age, gender, center and anti-CCP status. The proportion of patients in each treatment arm with MRI erosive progression after 2 years was calculated, using the smallest detectable change (0.61) as cut-off. <h3>Results</h3> Demographic composition was comparable to the ARCTIC primary sample. There were no statistically significant baseline differences between the arms in either of the combined MRI scores. The mean combined MRI inflammation score decreased during the first year (1-year change in ultrasound arm −10.8 (95% CI: −12.0 to −9.6), conventional arm −10.3 (95% CI: −11.5 to −9.0), p=0.56), and maintained at the same level throughout the 2<sup>nd</sup> year. There were no significant differences in changes from baseline between the study arms at any time (figure 1a). The mean combined MRI damage score showed a small increase over time, without any significant differences between study arms (figure 1b). In the ultrasound arm 45% of patients had MRI erosive progression vs. 39% in the conventional arm (OR: 1.26 (95% CI: 0.73 to 2.16), p=0.40). <h3>Conclusion</h3> A tight control strategy incorporating ultrasound information in treatment decisions did not lead to improved MRI inflammation or less structural damage, compared to a conventional tight control strategy. The findings support the conclusion of the ARCTIC trial that systematic use of ultrasound does not provide added value in the follow-up of patients with early RA treated according to current recommendations. <h3>References</h3> [1] E. A. Haavardsholm, et al. BMJ2016; 354: i4205 [2] J. Dale, et al. ARD2016; 75: 1043-50 [3] M. Østergaard, et al. J Rheum2017; 44: 1706-12 <h3>Disclosure of Interests</h3> Ulf Sundin: None declared, Anna-Birgitte Aga Consultant for: UCB, AbbVie, and Pfizer, Paid instructor for: UCB, Øivind Skare: None declared, Lena B Norberg: None declared, Till Uhlig Consultant for: Grünenthal, Novartis, Speakers bureau: Grünenthal, Novartis, Hilde Berner Hammer Grant/research support from: AbbVie, Pfizer and Roche, Paid instructor for: AbbVie, Pfizer, UCB, Novartis, Roche, Speakers bureau: AbbVie, Pfizer, UCB, Novartis, Roche, Désirée van der Heijde Consultant for: AbbVie, Amgen, Astellas, AstraZeneca, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Daiichi, Eli-Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, Union Chimique Belge, Tore K. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB., Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi, Mylan and UCB, Speakers bureau: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi and UCB, Siri Lillegraven: None declared, Espen Haavardsholm Grant/research support from: Pfizer, UCB, Roche, MSD, and AbbVie, Consultant for: Pfizer, Paid instructor for: Pfizer, Speakers bureau: Pfizer, UCB, Roche, and AbbVie