Objective In rheumatoid arthritis (RA), MRI provides earlier detection of structural damage than radiography (X-ray) and more sensitive detection of intra-articular inflammation than clinical examination. This analysis was designed to evaluate the ability of early MRI findings to predict subsequent structural damage by X-ray.
Methods Pooled data from four randomised controlled trials (RCTs) involving 1022 RA hands and wrists in early and established RA were analysed. X-rays were scored using van der Heijde-modified or Genant-modified Sharp methods. MRIs were scored using Outcome Measures in Rheumatology (OMERACT) RA MRI Score (RAMRIS). Data were analysed at the patient level using multivariable logistic regression and receiver operating characteristic curve analyses.
Results Progression of MRI erosion scores at Weeks 12 and 24 predicted progression of X-ray erosions at Weeks 24 and 52, with areas under the curve (AUCs) of 0.64 and 0.74, respectively. 12-week and 24-week changes in MRI osteitis scores were similarly predictive of 24-week and 52-week X-ray erosion progressions; pooled AUCs were 0.78 and 0.77, respectively. MRI changes in synovitis at Weeks 12 and 24 also predicted progression of X-ray joint damage (erosion and joint-space narrowing) at Weeks 24 and 52 (AUCs=0.72 and 0.65, respectively).
Conclusions Early changes in joint damage and inflammation detected with MRI predict changes in joint damage evident on subsequent X-rays. These findings support the use of MRI as a valid method for monitoring structural damage in short-duration RCTs.
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Handling editor Tore K Kvien
Funding Independent grant support was provided by Bristol-Myers Squibb, Genentech/Roche, Janssen and Pfizer. Data were provided by Amgen, Genentech/Roche and Janssen.
Competing interests CP, JDC, PC report other from Spire Sciences, Inc. outside the submitted work; VS, MØ report grants from Bristol-Myers Squibb, grants from Genentech/Roche, grants from Janssen R&D and grants from Pfizer during the conduct of the study; consulting fees from Abbvie; Amgen; AstraZeneca; Bayer; Boehringer-Ingelheim; Bristol-Myers Squibb, Celltrion, Crescendo/Myriad Genetics, Genentech/Roche, GlaxoSmithKline, Janssen, Lilly, Merck, Novartis, Pfizer, Regeneron, Samsung, Sandoz, Sanofi, UCB outside the submitted work; reports grants from Bristol-Myers Squibb, grants from Genentech/Roche, grants from Janssen R&D and grants from Pfizer during the conduct of the study; speaking or consulting fees from Abbvie, Bristol-Myers Squibb, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB, Wyeth; AD reports grants from Eli Lilley, Glaxo-Smith Kline, Janssen, Novartis, Pfizer, UCB outside the submitted work; RL reports other from Rheumatology Consultancy BV outside the submitted work; VKR reports personal fees from Bristol-Myers Squibb, grants from Genentech and grants from Pfizer outside the submitted work; OT reports grants and personal fees from Abbvie, Amgen, Bristol-Myers Squibb, Novartis, Pfizer and Roche/Genentech outside the submitted work; PGC is supported in part by the National Institute for Health Research (NIHR) Leeds Musculoskeletal Biomedical Research Unit. PGC also reports speakers bureau or consulting fees from Abbvie, Bristol-Myers Squibb, Lilly, Novartis, Pfizer and Roche.
Ackowledgement The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.
Patient consent Obtained.
Ethics approval This was a post hoc blinded analysis and ethical approval was obtained for the four included studies. All studies were conducted in accordance with the ethical principles of the Declaration of Helsinki.
Provenance and peer review Not commissioned; externally peer reviewed.
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