Management of arthropathy in inflammatory bowel diseases

Therapeutic Advances in Chronic Disease - Tập 6 Số 2 - Trang 65-77 - 2015
Rosario Peluso1, Francesco Manguso2, Maria Vitiello3, Salvatore Iervolino4, Matteo Nicola Dario Di Minno5
1Rheumatology Research Unit, Department of Clinical Medicine and Surgery, University Federico II, Via Sergio Pansini 5, 80131 Naples, Italy
2Complex Operating Unit of Gastroenterology, AORN ‘A. Cardarelli’, Naples, Italy
3Rheumatology Research Unit and Department of Clinical Medicine and Surgery, University Federico II, Naples, Italy
4Rheumatology and Rehabilitation Research Unit ‘Salvatore Maugeri’ Foundation, Telese Terme (BN), Italy
5Department of Clinical Medicine and Surgery, University “Federico II”, Naples, Italy

Tóm tắt

The most common extra-intestinal manifestation in patients with inflammatory bowel disease (IBD) is articular involvement, with a prevalence ranging between 17% and 39%. It is frequently characterized by an involvement of the axial joints but may also be associated with peripheral arthritis. The target of therapy in the management of arthritis associated with IBD is to reduce the inflammation and prevent any disability and/or deformity. This requires active cooperation between gastroenterologist and rheumatologist. The treatment of axial involvement has focused on the combination of exercise with nonsteroidal anti-inflammatory drugs. Immunomodulators have been efficacious in patients with peripheral arthritis and other extra-intestinal manifestations, but they are not effective for the treatment of axial symptoms of spondylitis. Tumor necrosis factor (TNF) α inhibitors have been proven to be highly effective in the treatment of IBD patients which are steroid-dependent or refractory to conventional therapy and in patients with associated articular manifestations. The treatment of peripheral involvement and/or enthesitis and/or dactylitis is based on local steroid injections, while sulfasalazine and/or low doses of systemic steroids may be useful in case of inadequate response to intra-articular steroids. Sulfasalazine induces only a little improvement in peripheral arthritis. Immunomodulators such as methotrexate, azathioprine, cyclosporine and leflunomide show their efficacy in some patients with peripheral arthritis and other extra-intestinal components. TNF-α inhibitors should be considered the first-line therapeutic approach when moderate-to-severe luminal Crohn’s disease or ulcerative colitis is associated with polyarthritis. The aim of this review is to provide a fair summary of current treatment options for the arthritis associated with IBD.

Từ khóa


Tài liệu tham khảo

10.1016/S0049-0172(03)00136-7

10.1111/jgh.12352

10.1016/j.rcl.2012.04.010

10.1542/peds.2009-3395

10.1007/s10067-009-1340-7

10.3748/wjg.15.2469

10.1056/NEJMoa020888

10.1053/berh.2002.0249

10.1053/sarh.2001.19960

10.1007/s11926-012-0282-2

10.1002/ibd.20196

10.7326/0003-4819-127-8_Part_1-199710150-00007

10.1002/art.1780070113

10.1001/jama.295.19.2275

10.1136/annrheumdis-2012-203075

10.1002/art.22669

10.1136/ard.2011.151027

10.1177/1759720X14535512

10.1136/ard.17.2.169

10.2174/138945011796818252

10.1097/MIB.0b013e318281f28f

10.1002/1529-0131(199911)42:11<2325::AID-ANR10>3.0.CO;2-C

10.1111/j.1572-0241.1999.01149.x

10.1053/j.gastro.2006.11.041

10.1136/bmj.39547.603218.AE

Dagfinrud H., 2005, J Rheumatol, 32, 1899

10.1056/NEJM197309062891001

10.1007/s000110050558

10.1517/14712598.8.7.1011

10.1016/j.crohns.2009.12.002

10.1055/s-0032-1306433

10.3899/jrheum.110741

10.1136/gut.14.12.923

10.1136/ard.61.suppl_3.iii40

10.1097/00124743-200104000-00002

10.1093/rheumatology/28.2.134

10.1016/j.gtc.2004.03.001

Ferraz M., 1990, J Rheumatol, 17, 1482

10.1136/ard.2003.012450

10.1002/art.23940

10.1002/ibd.20215

10.1136/annrheumdis-2011-200350

10.1136/ard.2003.019174

10.1016/S0140-6736(02)08512-4

10.1111/j.1365-2036.2010.04360.x

10.1016/j.semarthrit.2008.06.004

10.1111/j.1572-0241.2002.06064.x

10.1093/rheumatology/28.5.414

10.1002/art.23969

10.1053/j.gastro.2005.03.003

10.1136/gut.2004.049460

10.1097/01.mcg.0000170735.43887.3a

10.1007/BF02056956

10.1007/s00296-004-0467-8

10.1038/ajg.2011.64

Lambert R., 2009, J Rheumatol, 36, 3

10.1111/j.1365-2036.2010.04466.x

10.1111/j.1572-0241.2004.04039.x

10.1007/s00384-004-0626-0

10.1136/ard.62.1.74

10.1136/bmj.2.5355.483

10.1111/j.1365-2230.1994.tb02699.x

10.2217/imt.12.85

10.4065/76.1.84

10.1002/1529-0131(200112)44:12<2862::AID-ART474>3.0.CO;2-W

10.1016/j.crohns.2014.01.006

10.1002/ibd.20230

10.1517/14712598.2014.885945

10.1007/s10620-008-0481-x

10.3109/s10165-010-0279-5

10.1111/j.1572-0241.2000.02241.x

10.1002/ibd.21468

10.1016/j.autrev.2014.04.003

10.1136/gut.42.3.387

10.1016/j.dld.2010.07.010

10.1097/00124743-199806000-00007

10.1007/s00296-006-0148-x

Peluso R., 2009, Reumatismo, 61, 15

10.1007/s10067-013-2252-0

10.3899/jrheum.120415

10.1155/2013/631408

10.1177/1721727X1401200204

10.1056/NEJM199905063401804

10.1136/gut.51.4.536

10.1097/00004836-200012000-00004

10.1080/03009740510026698

10.1136/ard.2008.094946

10.1093/rheumatology/41.11.1330

10.1097/MIB.0b013e31827eea78

10.1016/j.cgh.2010.04.021

10.1053/j.gastro.2008.07.014

10.1053/j.gastro.2013.06.010

10.1056/NEJMoa067594

10.1053/gast.2001.28674

10.1053/j.gastro.2009.06.061

10.1016/j.cgh.2005.12.002

Sanduzzi A., 2012, J Rheumatol, 89, 82

10.1002/1529-0131(200112)44:12<2728::AID-ART459>3.0.CO;2-8

Soscia E., 2009, J Rheumatol, 83, 42

10.1136/bmj.2.5054.1157

10.1016/S0016-5085(19)34904-2

Sutherland L., 2006, Cochrane Database Syst Rev, 2, CD000544

10.1038/nm763

Thomson G., 1994, J Rheumatol, 21, 570

10.1016/S0140-6736(00)03239-6

10.1002/art.21913

10.1136/ard.2011.151563

10.1097/01.MIB.0000209787.19952.53

10.1053/j.gastro.2006.03.028

Voulgari P., 2011, Ann Gastroenterol, 24, 173

10.1007/s11894-008-0108-6

Wright V., 1976, Seronegative Polyarthritis

10.1038/ajg.2011.63

10.4103/1319-3767.87177