Axial Spondyloarthritis (Oxford Rheumatology Library) by Stefan Siebert, Raj Sengupta, Alexander Tsoukas

By Stefan Siebert, Raj Sengupta, Alexander Tsoukas

Axial spondyloarthritis is the most typical inflammatory arthritis affecting the backbone. in general first offering to quite a few basic and secondary care execs, the excessive international illness burden of this situation has created a necessity for elevated information of this throughout a number rheumatology specialties.

A pocketbook geared toward the non-specialist reader Axial Spondyloarthritis is the basic consultant to this universal situation. concentrating on the sensible implications of advancements in class, prognosis and remedy, this simply obtainable textual content absolutely covers the wider spectrum of the disease.

Concise and completely illustrated, this addition to the Oxford Rheumatology Library covers the historical past and pathophysiology of axial spondylitis, along distinct sections on remedies, problems and manifestations of the situation. With every one part supported through a convenient key issues part, Axial Spondyloarthritis is an invaluable and optimistic source for any practitioner or trainee encountering this condition.

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It has been long recognized that there are many patients in the community with axSpA who remain undiagnosed. Therefore, it had been hoped that, despite being developed as classification criteria, the various IBP criteria could be used to facilitate screening for IBP, particularly in primary care settings. Despite significant efforts to increase the awareness of healthcare professionals about the concept of IBP, knowledge of IBP features remains limited in primary care. A UK study reported that 17% of primary care doctors were able to identify fewer than four features suggestive of IBP, although there is likely to be significant regional and national variation in awareness of IBP in primary care settings.

In addition to IL23R, these genes include IL12B, TYK2, IL6R, and IL27. However, understanding the therapeutic implications of susceptibility genes identified by GWAS is not without challenge, as demonstrated by IL6R. This gene has been identified and confirmed by GWAS studies as a susceptibility gene for AS, but in clinical trials, the anti-​IL-​6R antibodies tocilizumab and sarilumab did not improve clinical outcomes in AS, despite reducing CRP levels. Therapies targeting IL-​23 and IL-17 are addressed in the section on pharmacological therapies (Chapter 15).

These and other observations led to the enthesitis-​based model of SpA pathogenesis. An elegant study demonstrated that in a TNF-​dependent mouse model, the development of enthesitis and subsequent new bone formation are dependent on continuous biomechanical strain (Jacques, 2013). None of the mice whose hind legs were ‘unloaded’ by being suspended by their tails, developed hind leg arthritis while all the weight-​bearing control mice developed severe enthesitis. How best to address the issue of biomechanical stress as potential trigger of AS is not clear in clinical practice, but requires further study as this has implications for how and when best to deliver physical therapy interventions in these conditions.

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