Abstract
Spondyloarthritis (SpA) comprises a group of diseases characterized by axial, entheseal, and peripheral joint inflammation in the setting of overlapping nonmusculoskeletal inflammatory manifestations (skin, eye, and gut) and a tendency toward familial aggregation. Typically, autoantibodies are not formed in patients with SpA. The group of diseases includes axial spondylitis (AxSpA), of which ankylosing spondylitis (AS) is the most severe form, and peripheral spondylarthritis, which includes reactive arthritis, psoriatic arthritis (PsA), enteropathic arthritis, and “undifferentiated spondyloarthritis.” Susceptibility to AxSpA has a strong genetic component. In total, over 133 genes have been identified for AS, more than 60 for psoriasis/psoriatic arthritis, and nearly 200 for inflammatory bowel disease. The most commonly recognized genetic factor is the human leukocyte antigen (HLA)-B27, associated especially with AxSpA and PsA. Some susceptibility genes are involved in the T-helper 17 (Th17) and antigen-processing/-presenting pathways. The development of classification criteria and advances in imaging allow for earlier diagnosis. Striking advances have also occurred in treatment with the introduction of biological therapies, such as anti–tumor necrosis factor (TNF), interleukin-17 (IL-17), interleukin-23 (IL-23), and Janus kinase inhibitor therapies.
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