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 ankylosing spondylitis (AS), reactive arthritis, psoriatic arthritis, enteropathic arthritis, and “undifferentiated spondyloarthritis.” Susceptibility to SpA has a strong genetic component. In addition to human leukocyte antigen (HLA)-B27, 70 genes have been identified for AS, 60 for psoriasis/psoriatic arthritis, and 130 for inflammatory bowel disease. Some susceptibility genes are involved in the T-helper 17 (Th17) and antigen-processing/-presenting pathways. The development of new classification criteria and of advances in imaging allow for earlier diagnosis. Striking advances have also occurred with treatment, with the introduction of biological therapies, such and anti–tumor necrosis factor (TNF) and interleukin-17 (IL-17) therapies.
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