Abstract
Chronic inflammatory arthritis, a hallmark of a variety of inflammatory rheumatic diseases and inflammatory bowel disease, is a lifelong condition, often with onset in early adulthood, with an important morbidity and even mortality in our society. It is estimated that approximately 2–3% suffers from chronic arthritis in our society. The coexistence of gut and joint inflammation is well established in spondyloarthritis (SpA), a cluster of interrelated rheumatologic diseases, characterized by a number of clinical and genetic features including peripheral arthritis (typical of lower limb joints) as well as inflammation of the axial skeleton (e.g., spine). Remarkably, other organs including skin (psoriasis) or the eye (anterior uveitis) may also be affected, indicating the systemic nature of these diseases. Various subtypes of SpA can be distinguished based upon clinical features, but an important overlap between them exists. The clinical subtypes include an kylosing spondylitis (AS, characterized by prominent inflammation of the axial skeleton – spine, sacroiliac joints, although other joints may also be affected), infection triggered reactive arthritis, some forms of juvenile chronic arthritis, arthritis in association with inflammatory bowel diseases (IBD), and some types of psoriatic arthritis.
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Elewaut, D., Jacques, P., Melis, L., Venken, K. (2011). Mechanisms Regulating TNF-Driven Gut and Joint Inflammation. In: Wallach, D., Kovalenko, A., Feldmann, M. (eds) Advances in TNF Family Research. Advances in Experimental Medicine and Biology, vol 691. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6612-4_42
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DOI: https://doi.org/10.1007/978-1-4419-6612-4_42
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