Objective: Anti-tumor necrosis factor (TNF) therapies provide symptomatic benefit in patients with spondyloarthropathy (SpA). Their effect on structural lesions has not yet been assessed. Biochemical markers of cartilage turnover revealing type II collagen degradation and synthesis are associated with joint damage in rheumatoid arthritis; their role in SpA is unknown. We describe the effects of etanercept on biochemical markers of type II collagen synthesis and degradation in patients with SpA followed for 2 years.
Methods: A total of 29 patients with SpA aged 22-68 years were included in a prospective 2-year study. Each patient received etanercept (25 mg twice a week) because of active disease despite optimal treatment. Cartilage degradation was investigated by measuring serum levels of the type II collagen fragments Helix-II and C2C, whereas the C-terminal propeptide of type II collagen (PIICP) was used as a marker of type II collagen synthesis. These markers were measured at baseline and after 1, 3, 6, 12, and 24 months of treatment.
Results: Over 2 years, there was a significant decrease of serum C2C (p = 0.0035 by repeated Friedman's test) and serum Helix-II (p = 0.004). Compared to baseline, the decrease of serum C2C was significant at Month 12 (-12.1%; p = 0.004), whereas the decrease of serum Helix-II was observed as early as 1 month (-18.1%; p = 0.015) after start of therapy, reaching a maximum decrease of -33.4% (p = 0.0079) at Month 12. Conversely, PIICP increased significantly by 17% (p = 0.006) at 24 months.
Conclusion: These data suggest that etanercept may have beneficial effects on cartilage metabolism in patients with SpA.