Abstract

Rheumatic symptoms are the most common extra-intestinal manifestations of inflammatory bowel diseases (IBD). Both ulcerative colitis and Crohn disease (1)(2) can be complicated by seronegative spondyloarthropathies, including two principal patterns of arthritis: spondylitis and peripheral arthritis. Spondyloarthropathies resembling idiopathic ankylosing spondylitis occur in 10% of patients with ulcerative colitis and, less frequently, in those with Crohn disease; peripheral, often asymmetric, arthropathies occur in 5–20% of IBD patients. Unlike arthropathy limited to five or fewer joints, polyarthropathy and spondyloarthropathies do not reflect the activity of the underlying IBD. The “gold standard” for assessing joint damage remains the plain radiograph, which images only the bone and allows reliable detection of changes within a time span of at least 12 months. Importantly, all such techniques image only damage that has already occurred. Even after repeated investigations, they are of limited use in informing the clinician of continuing or future damage. Biochemical markers may provide a valuable tool for the frequent quantitative measurements required for the diagnosis and monitoring of joint disease. Highly sensitive C-reactive protein (CRP) assays provide information on the inflammatory process (3) but are poor markers for joint disease in IBD. Other markers for joint disease have been proposed (4) that are related to structures within joints. The concentrations of YKL-40 in serum and synovial fluid are closely correlated in patients with joint disease (5), suggesting that most of the protein found in serum may be produced within the joint (6)(7). YKL-40 is produced not only by chondrocytes and synovial cells but also by macrophages, neutrophils, cancer cells, endothelial cells, smooth muscle cells in blood vessels, and by cells (probably hepatic stellate cells) in the fibrotic liver (8)(9)(10)(11)(12)(13). The protein is a growth factor for fibroblasts, chondrocytes, …

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