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No efficacy of anti-IL-23 therapy for axial spondyloarthritis in randomised controlled trials but in post-hoc analyses of psoriatic arthritis-related ‘physician-reported spondylitis’?
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  • Published on:
    Correspondence on “No efficacy of anti-IL-23 therapy for axial spondyloarthritis in randomised controlled trials but in post-hoc analyses of psoriatic arthritis-related ‘physician-reported spondylitis’?”.
    • Stefan Siebert, Professor of Inflammation Medicine and Rheumatology University of Glasgow, Glasgow, United Kingdom
    • Other Contributors:
      • Helena Marzo-Ortega, Consultant Rheumatologist and Honorary Clinical Associate Professor

    We read with interest the Viewpoint article by Braun and Landewé regarding post-hoc analysis of back pain in trials of IL-23 inhibitor therapy in patients with peripheral psoriatic arthritis (PsA) [1]. Indeed, we share their concerns regarding study design, the use of outcome measures developed for axial spondyloarthritis (axSpA) and, most importantly, the attribution of the diagnostic label “physician-reported spondylitis” in these patients. In addition to the issues eloquently outlined in the article, it is important to be aware that the pre-test probability of inflammatory disease being directly responsible for back pain is likely much lower in patients with PsA who are older, and therefore more likely to have mechanical or non-specific back pain, than people presenting with axSpA. In other words, even before doing any test, a middle-aged person with PsA, as represented in most phase III PsA clinical trials, is more likely to have non-inflammatory than inflammatory back pain. These “causes” of back pain do of course co-exist and are not easily distinguished by clinical or imaging assessments. For example, disc and degenerative spinal disease can lead to apparent inflammatory features, such as bone marrow oedema on magnetic resonance imaging [2, 3] that are likely a secondary response to altered biomechanical stresses rather than primary inflammatory disease and therefore unlikely to be responsive to biologic therapies. Furthermore, imaging data on the prevalence and na...

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    Conflict of Interest:
    S Siebert S. Siebert has received institutional research funding from Amgen (previously Celgene), Boehringer Ingelheim, BMS, Eli Lilly, Janssen, and UCB and honoraria/speaker fees from AbbVie, Biogen, Celgene, GSK, Janssen, Novartis and UCB.
    H Marzo-Ortega has received research funding from Janssen, Novartis and UCB, and speaker fees and/or honoraria from AbbVie, Biogen, Celgene, Eli-Lilly, Moonlake, Novartis, Pfizer, Takeda and UCB.