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Spondyloarthritis (SpA) is a chronic immune-mediated inflammatory disease with diverse phenotypic manifestations including spondylitis, arthritis, enthesitis and extra-articular manifestations (psoriasis, uveitis, inflammatory bowel disease). The common genetic risk factors, the strong familial aggregation and the overlapping immunopathology suggest that these different phenotypic manifestations share common pathogenic pathways. This concept is further strengthened by the good clinical response of all different SpA manifestations to TNF-blocking therapies. However, the phenotypic diversity of SpA is still a major challenge in properly diagnosing, classifying and monitoring the disease and may lead to undertreatment of less typical SpA cases such as undifferentiated SpA. The optimal use of current treatments and the development of novel therapies, including compounds targeting the IL-23/IL-17 axis, thus requires a detailed understanding of both the clinical presentation and the underlying pathogenic pathways in SpA.
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Paramarta et al. (2013) studied this question.
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