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Increased urinary type II collagen helical and C telopeptide levels are independently associated with a rapidly destructive hip osteoarthritis.

Garnero P, Charni N, Juillet F, Conrozier T, Vignon E

Molecular Markers, Synarc, Lyon, France. patrick.garnero@synarc.com

OBJECTIVES: Biochemical markers reflecting the degradation of the type II collagen helical (Helix-II) and type II collagen C telopeptides (CTX-II) have been developed. Aim: To investigate the association of rapidly destructive hip osteoarthritis with urinary Helix-II and urinary CTX-II. PATIENTS AND METHODS: 12 patients (mean age 70 years) meeting the criteria for rapidly destructive hip osteoarthritis and 28 patients with slowly progressive hip osteoarthritis (mean age 63 years) defined as <0.20 mm joint space loss/year were included in a case-control study. In each patient, urinary Helix-II and CTX-II were measured at the end of the follow-up period, with retrospective evaluation of x rays. RESULTS: Helix-II levels were 41% (p = 0.002) higher in the 40 patients with hip osteoarthritis than in 75 healthy controls. Increased Helix-II levels were associated with decreased minimum joint space width of the hip (r = -0.57, p = 0.001). Mean urinary Helix-II levels were 71% higher in rapidly destructive than in slowly progressive disease (mean (standard deviation (SD)) ng/mmol Cr: 396 (160) v 232 (118) ng/mmol; p = 0.002). When levels of Helix-II and CTX-II in the highest tertile were both included in a multivariate logistic regression model, high Helix-II level (OR; (95% CI) 5.73 (1.01 to 32.8)) after adjustment for age and body mass index and high CTX-II level (6.67 (1.14 to 39.0)) were, independently of each other, associated with a rapidly destructive disease. CONCLUSION: Increased urinary Helix-II levels are associated with rapidly destructive hip osteoarthritis, independently of urinary CTX-II. Measurement of Helix-II, alone or in combination with CTX-II, could be useful for the clinical investigation of patients with hip osteoarthritis.

Published 19 November 2006 in Ann Rheum Dis, 65(12): 1639-44.
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