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Current Rheumatology Reviews

Editor-in-Chief

ISSN (Print): 1573-3971
ISSN (Online): 1875-6360

Rheumatic Manifestations Associated with Inflammatory Bowel Diseases

Author(s): Marta Podswiadek, Renata D'Inca, Giacomo Carlo Sturniolo, Francesca Oliviero and Leonardo Punzi

Volume 3, Issue 1, 2007

Page: [47 - 56] Pages: 10

DOI: 10.2174/157339707779815731

Price: $65

Abstract

Rheumatic manifestations, in particular joint complaints, are frequent features in inflammatory bowel disease (IBD), with a prevalence varying from 10 to 35%. Their spectrum is almost wide, involving bone, tendons, entheses and joints. Joint manifestations may be seen as arthralgia and/or inflammatory arthropathies. These latter may in turn be found in three principal forms: the peripheral, the axial or spondylitis and that overlapping between these two varieties. Peripheral arthritis may be classified in oligoarticular (type I) and polyarticular (type II) forms. Oligoarthritis is the most frequent. Usually asymmetric, involving large joints of lower limbs, it is transient, commonly associated with IBD flares, and may disappear after few weeks, although in 10% of cases it may evolves to chronic arthritis. Type II arthritis is polyarticular and symmetric, involving hands and feet but also large joints. The prevalence is about 2-4% of IBD patients, its course is independent from IBD flares and usually evolves in chronic disease. Peripheral arthritis is classically nondeforming, non erosive, and seronegative for the rheumatoid factor. Axial involvement is equally frequent in both CD and UC and varies in different studies from 10 to 30% for sacroiliitis and from 3 to 10% for ankylosing spondylitis. Its course is independent from IBD state, the extension of IBD involvement and the occurrence of flares. The treatment of rheumatic manifestations in IBD is frequently problematic, due to the possibility of frequent side effects. Among drugs used for IBD, corticosteroids, also effective in joint complaints, may have osteopenic effects; sulfasalazine, sometimes able to control peripheral arthritis, is ineffective for the axial involvement. A potential gut toxicity is associated with the use of NSAIDs, which in some patients may induce asymptomatic lesions causing small gut bleeding and loss of proteins. Local injections with steroid may be used for tendonitis, monoarthritis or isolated sacroiliac inflammation. In patients with peripheral arthritis, especially when involving several joints and/or refractory to other therapies, disease modifying drugs for rheumatoid arthritis (DMARDs) should be used. Among these, methotrexate is also useful for CD while it seems inefficacious in UC. Cyclosporin, administrated alone or in association, may contain flares of steroid refractory UC. Azathioprine is commonly used to induce and maintain remission in refractory CD while its role on arthritis is marginal. Aminobisphosphonates seem effective for both axial and peripheral involvements and probably, it may represent a good option for the future in the management of enteropathic arthritis, because of their anti-osteopenic effect. Finally, the most promising opportunities derive from the recently introduced biologic agents, in particular anti-tumour necrosis factor (TNF) . Infliximab, a chimeric anti-TNFα monoclonal IgGI antibody, has largely demonstrated its efficacy in refractory CD and in all rheumatic manifestations. Other biologic agents are proposed, including the human anti-TNF monoclonal antibody adalimumab, antibodies to integrins (anti-α 4 β7), anti-ICAM-1 (intracellular adhesion molecule 1) and IL-10. Concerning the surgical options, the colectomy may be protective on type I peripheral arthritis but is not influent on the course of axial disease, while the surgery on small intestine usually do not prevent the appearance of peripheral arthritis. In the case of destructive arthritis, like coxitis, joint prosthesis may be necessary.

Keywords: Inflammatory bowel disease, Crohn's disease, ulcerative colitis, enteroarthritis, arthritis, heumatic manifestations, anti-TNF therapy


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