Spondyloarthropathies Ankylosing Spondylitis

T cells are also thought to play an important role in the pathogenesis of the spondyloarthropathies, a group of seronegative inflammatory conditions that mainly affect the axial skeleton. Ankylosing spondylitis is the prototype spondyloarthropathy characterized by spinal inflammation, radiologic evidence of sacroiliitis and spondylitis, arthritis, and soft tissue inflammation, including enthesopathy (van der Linden et al. 2005). A number of findings implicate TNF-a in the pathogenesis of ankylosing spondylitis, including the development of an ankylosing spondylitis-like syndrome in mice expressing a truncated form of the TNF gene, higher serum levels of TNF in patients with ankylosing spondylitis relative to patients with noninflammatory back pain, and the detection of TNF-a mRNA in sacroiliac joint specimens from patients with ankylosing spondylitis (Braun et al. 1995; Davis 2005).

Studies conducted in patients with ankylosing spondylitis have generally evaluated the effects of etanercept on clinical end points, and therefore pharmacodynam-ic data in this condition are somewhat limited. Etaner-cept has been shown to modify markers of cartilage turnover in patients with ankylosing spondylitis via reduced type II collagen degradation and increased aggrecan turnover (Maksymowych et al. 2005). Sixteen weeks' treatment with etanercept (25 mg twice weekly) significantly reduced levels of C2C epitope, a biomark-er of cartilage turnover (marker of type II collagen degradation by collagenase), in patients with ankylosing spondylitis. This change correlated with reductions in CRP and ESR (Maksymowych et al. 2005).

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