By Stefan Siebert, Raj Sengupta, Alexander Tsoukas
Axial spondyloarthritis is the most common inflammatory arthritis affecting the backbone. often first providing to a number of basic and secondary care execs, the excessive international ailment burden of this situation has created a necessity for elevated knowledge of this situation throughout more than a few rheumatology specialties.
A pocketbook geared toward the non-specialist reader Axial Spondyloarthritis is the basic consultant to this universal . targeting the sensible implications of advancements in type, prognosis and remedy, this simply obtainable textual content totally covers the wider spectrum of the disease.
Concise and entirely illustrated, this addition to the Oxford Rheumatology Library covers the background and pathophysiology of axial spondylitis, along specified sections on remedies, problems and manifestations of the . With each one part supported via 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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Additional resources for Axial spondyloarthritis
However, the recognition that syndesmophytes were more likely to develop at the sites of resolved corner inflammatory lesions rather than sites of persistent lesions, led to the ‘TNF brake’ hypothesis. g. in response to treatment with TNF inhibitors), the brake is released, allowing tissue repair and new bone formation to occur. As a result of this uncoupling between inflammation and new bone formation, patients who otherwise respond well to anti-TNF therapy may appear to have radiographic progression due to the new bone formation (which would have occurred in many anyway, but at a later date, in the absence of TNF inhibition).
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). In summary, despite the strong heritability of AS and significant progress in identifying the susceptibility genes, this is a complex, multigenic disease where different combinations of risk loci interact with each other and with environmental and other factors to yield the clinical phenotype observed in an individual patient.
Homodimerization theory HLA-B27 heavy chains have a propensity to self-associate and homodimerize, resulting in the expression of homodimers on the cell surface which can be recognized by receptors on Th17 and natural killer cells, resulting in IL-17 production. 1). Other MHC genes (such as HLA-B60) have been implicated but in many cases these have been confounded by linkage to HLA-B27 or not been replicated in other cohorts. 1), with the most notable pathways including: 1. g. interleukin (IL)-1, IL-1 receptor 2.
Axial spondyloarthritis by Stefan Siebert, Raj Sengupta, Alexander Tsoukas