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Andrew Keat
1Department of Rheumatology, Northwick Park Hospital, Harrow, UK
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Andrew Keat the 1 last update 2020/07/07
Rheumatology, Volume 53, Issue suppl_1, April 2014, Pages i15–i16, https://doi.org/10.1093/rheumatology/keu067.001
03 April 2014
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Both reactive arthritis (ReA) and enteropathic arthritis (EntA) are defined by clinical descriptions without clear diagnostic criteria; in each case pathogenesis is assumed to involve infective agents, genitourinary or intestinal inflammation. Being members of the SpA family, both conditions typically present with characteristic SpA lesions including large joint oligoarthritis, enthesitis, dactylitis or inflammatory back pain associated with sacroiliitis. EntA may also manifest as a symmetrical small joint polyarthritis (type 2) that may be difficult to differentiate from RA. Musculoskeletal lesions may be accompanied by psoriasiform skin lesions and a past history of iritis is common. As in other SpAs there is a higher than expected prevalence of HLA-B27 though the prevalence of other SpA-associated genes is less clear. ReA is associated epidemiologically with non-gonococcal infection of the genito-urinary tract and specific bacterial forms of diarrhoea. Sporadic reports of arthritis associated with a wide range of other infections are of uncertain significance. Potentially viable IA bacteria and bacterial elements have been identified in patients with ReA and similar conditions but their pathogenic significance remains subject to debate. Enteropathic arthritis may be associated with either Crohn’s disease or ulcerative colitis though arthritis has also been reported in patients with coeliac disease, collagenous colitis and Whipple’s disease. Family studies suggest that the link between the bowel disease and the arthritis may be genetic rather than bacterial and low grade IBD is found in a high proportion of patients with all forms of SpA. However the interaction between gut microbiota, local cytokine production and inflammatory change at entheses and joints may be central to the pathogenesis of SpA. Treatment must take into account the usually self-limiting nature of ReA and the potential for NSAIDs to exacerbate IBD. In ReA anti-microbial treatment is essential for eradication of genital tract-infection in both patients and sexual partners but the use of antibiotics for treatment of arthritis is controversial. In patients with persistent ReA or EntA similar therapeutic approaches to those taken in RA, including use of DMARDs, are usually advocated though the evidence base is very limited. Surgical colectomy may benefit peripheral arthritis in some patients with ulcerative colitis but subsequent pouchitis in those with ileoanal pouches is not linked to exacerbation of arthritis. Activity of axial disease appears unrelated to activity of the bowel disease.

Disclosure statement: The author has declared no conflicts of interest.

© The Author 2014. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: [email protected]


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