Metsios, Giorgos S.; Stavropoulos-Kalinoglou, Antonios; Koutedakis, Yiannis; Kitas, George D. (Scientific Society of Evangelismos Hospital, 2006)
Rheumatoid arthritis is a chronic autoimmune disease characterised by joint pain and stiffness but also systemic mutli-organ involvement. Several features are due to excessive production of inflammatory cytokines, particularly tumour necrosis factor alpha, interleukin-1 and interleukin-6. These are implicated in both local synovial inflammation, which causes joint destruction, but also systemic inflammation, which can cause loss of body cell mass, amongst other phenomena. Body cell mass breakdown in rheumatoid arthritis leads to the classical, but largely ignored, metabolic abnormality known as rheumatoid cachexia. Cachexia is a very strong predictor of adverse functional outcome and death in many disease states. In this review we highlight the mechanisms linked with rheumatoid cachexia and discuss possible interventions that may limit this in patients with rheumatoid arthritis.
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