Effects of Etanercept on Serum Biochemical Markers of Cartilage Metabolism in Patients with Spondyloarthropathy

KARINE BRIOT, CHRISTIAN ROUX, LAURE GOSSEC, NADINE CHARNI, SAMI KOLTA, MAXIME DOUGADOS, and PATRICK GARNERO

ABSTRACT.

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. (First Release Jan 15 2008; J Rheumatol 2008;35:310-14)

Key Indexing Terms:

ETANERCEPT
CARTILAGE METABOLISM
SPONDYLOARTHROPATHY
COLLAGEN SYNTHESIS

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From the Faculté de Médecine, Université Paris-Descartes, UPRES-EA 4058, Hôpital Cochin, Paris; and INSERM U664 and Synarc, Lyon, France.

Supported by an unrestricted grant from Wyeth Pharmaceuticals, Paris, France.

K. Briot, MD; C. Roux, MD, PhD; S. Kolta, MD; L. Gossec, MD; M. Dougados, MD, PhD, Faculté de Médecine, Université Paris-Descartes, UPRES-EA 4058, Hôpital Cochin; N. Charni, PhD; P. Garnero, PhD, INSERM U664 and Synarc.

Address reprint requests to Dr. K. Briot, Department of Rheumatology, Cochin Hospital, 27 rue du Faubourg St. Jacques, 75014 Paris, France.

Accepted for publication September 30, 2007.

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