Axial spondyloarthritis: new advances in diagnosis and managementBMJ 2021; 372 doi: https://doi.org/10.1136/bmj.m4447 (Published 04 January 2021) Cite this as: BMJ 2021;372:m4447
- 1Allergy, Immunology & Rheumatology Division, University of Rochester Medical Center, Rochester, New York, USA
- 2Rheumatology, Allergy & Clinical Immunology Division, University of California, Davis, Shriners Hospital, Sacramento, California, USA
- Correspondence to C Ritchlin:
Axial spondyloarthritis (axSpA) is an inflammatory disease of the axial skeleton associated with significant pain and disability. Previously, the diagnosis of ankylosing spondylitis required advanced changes on plain radiographs of the sacroiliac joints. Classification criteria released in 2009, however, identified a subset of patients, under the age of 45, with back pain for more than three months in the absence of radiographic sacroiliitis who were classified as axSpA based on a positive magnetic resonance imaging or HLAB27 positivity and specific clinical features. This subgroup was labeled non-radiographic (nr)-axSpA. These patients, compared with those identified by the older New York criteria, contained a larger percentage of women and demonstrated less structural damage. However, their clinical manifestations and response to biologics were similar to radiographic axSpA. The discovery of the interleukin (IL) IL-23/IL-17 pathway revealed key molecules involved in the pathophysiology of axSpA. This discovery propelled the generation of antibodies directed toward IL-17A, which are highly effective and demonstrate treatment responses in axSpA that are similar to those observed with anti-TNF agents. The finding that agents that block IL-23 were not effective in axSpA came as a surprise and the potential underlying mechanisms underlying this lack of response are discussed. New agents with dual inhibition of the IL-17A and F isoforms and some oral small molecule agents that target the Jak-STAT pathway, have also shown efficacy in axSpA.
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Acknowledgments: The authors would like to thank Thanh Nguyen for assistance with graphic design, Johnny Monu for assistance with radiographic and MRI images, and Michael Weisman for his review of the manuscript.
Competing interests: All authors have completed the Unified Competing Interest form (available on request from the corresponding author) and declare: no support from any organization for the submitted work; no financial relationships with any organizations that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work. CR declares research funding: Abbvie, UCB, Amgen; consultant: Abbvie, Amgen, UCB, Lilly, Novartis, Gilead, BMS, Janssen, Pfizer. IA declares research funding: Pfizer, Tanabe Research Laboratories, Consultant Novartis.
No outside funding was received for preparation of this manuscript.
Provenance and peer review: commissioned; externally peer reviewed.