Primer | Published:

Axial spondyloarthritis

Nature Reviews Disease Primers volume 1, Article number: 15013 (2015) | Download Citation

Abstract

The term axial spondyloarthritis covers both non-radiographic disease and radiographic disease (also known as ankylosing spondylitis). Some studies have been performed to investigate the prevalence of axial spondyloarthritis, although most are limited to patients with radiographic disease. A strong genetic association has been shown between axial spondyloarthritis and human leukocyte antigen-B27 (HLA-B27), but the pathogenetic role of HLA-B27 has not yet been clarified. Tumour necrosis factor (TNF), IL-17, IL-23 and downstream pathways also seem to be important — based on the good results of therapies directed against these molecules — but their exact role in the inflammatory process is also not yet clear. Elucidating the interaction between osteoproliferation and inflammation will be crucial for the prevention of long-term structural damage of the bone. The development of new criteria for classification, diagnosis and screening of patients with axial spondyloarthritis will enable earlier intervention for this chronic inflammatory disease. MRI has become an important tool for the early detection of axial spondyloarthritis. NSAIDs and TNF blockers are effective therapies, including in the early non-radiographic stage. Therapeutic blockade of IL-17 or IL-23 seems to be a promising new treatment option. Tools for measuring quality of life in axial spondyloarthritis have become relevant to assess the impact that the disease has on patients. These diagnostic and therapeutic advances will continue to change the management of axial spondyloarthritis, and new insights into the disease pathogenesis will hopefully accelerate this process. For an illustrated summary of this Primer, visit: http://go.nature.com/51b1af

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Acknowledgements

The authors thank U. Kiltz and X. Baraliakos for their support in the preparation of this manuscript.

Author information

Affiliations

  1. Rheumatology, Charité, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany.

    • Joachim Sieper
  2. Rheumazentrum Ruhrgebiet, Herne, Germany.

    • Jürgen Braun
  3. Faculty of Medicine, Paris Descartes University, Department of Rheumatology, Hôpital Cochin, Assistance Publique, Hôpitaux de Paris, INSERM (U1153), Clinical Epidemiology and Biostatistics, PRES Sorbonne Paris-Cité, Paris, France.

    • Maxime Dougados
  4. Clinical Immunology and Rheumatology and Amsterdam Rheumatology and Immunology Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

    • Dominique Baeten

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Contributions

Introduction (J.S.); Epidemiology (M.D.); Mechanisms/pathophysiology (D.B.); Diagnosis, screening and prevention (J.S.); Management (J.B.); Quality of life (J.B.); Outlook (J.S.); overview of Primer (J.S.).

Competing interests

J.S. has received honoraria for being a member of speaker's bureau and/or consulting fees from the following companies: AbbVie Boehringer Ingelheim Janssen Lilly Merck Novartis Pfizer and UCB; and research grants from the following companies: AbbVie Janssen Merck and Pfizer. J.B. discloses no financial conflicts. M.D. has received honouraria for being a member of speaker's bureau and/or consulting fees from the following companies: AbbVie Boehringer Ingelheim Janssen Lilly Merck Novartis Pfizer and UCB; and his department has received research grants from the following companies: AbbVie Janssen Lilly Merck Pfizer Novartis and UCB. D.B. has received honouraria for being a member of speakers bureau and/or consulting fees from the following companies: AbbVie Pfizer MSD UCB Novartis Lilly Boehringer Ingelheim Roche Bristol–Myers Squibb Janssen Glenmark Zymetech and FivePrime.

Corresponding author

Correspondence to Joachim Sieper.

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https://doi.org/10.1038/nrdp.2015.13