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Retinol (Vitamin A) and Retinol-Binding Protein Levels Are Decreased in Ankylosing Spondylitis: Clinical and Genetic Analysis

FINBAR D. O'SHEA, FLORENCE W.L. TSUI, BASIL CHIU, HING WO TSUI, MEHRDAD YAZDANPANAH, and ROBERT D. INMAN

ABSTRACT.

Objective.
Retinol (vitamin A) plays an important role in bone structure and function. Treatment with retinoids has been associated with bone abnormalities mimicking spondyloarthropathy and diffuse idiopathic skeletal hyperostosis. To determine whether retinol concentrations are altered in patients with ankylosing spondylitis (AS), we examined serum retinol levels in patients with AS and healthy controls.

Methods. Retinol was assessed using mass spectrometry, and retinol-binding protein levels were assessed by ELISA. Retinol levels were correlated with clinical disease activity indices. The CYP26 gene, which plays a key role in retinol metabolism, was examined to define any single-nucleotide polymorphisms (SNP) associations with AS.

Results. Retinol levels were significantly lower in the AS cohort than in controls (mean 2.39 ± 0.88 µmol/l for AS, 3.34 ± 1.01 µmol/l for controls; p < 0.0001). Retinol-binding protein levels were also lower in AS than controls (AS 4.65 ± 2.10 µg/l; controls 7.48 ± 4.87 µg/l; p < 0.001). Serum retinol levels did not correlate with indices of disease activity defined serologically (C-reactive protein, erythrocyte sedimentation rate) or clinically (Bath AS Disease Activity Index, Bath AS Functional Index). Genetic analysis showed that an exonic CYP26C1 SNP (rs11187265) is not associated with AS.

Conclusion. The hallmark of AS is neo-ossification. AS is associated with abnormal serum levels of retinol, a biochemical factor linked to pathological hyperostosis. Further genetic studies are warranted into the genetic basis of the retinol-AS relationship. (First Release Nov 15 2007; J Rheumatol 2007;34:2457-9)

Key Indexing Terms:

ANKYLOSING SPONDYLITIS
DISEASE ACTIVITY
GENETIC STUDIES
RETINOL
RETINOL BINDING PROTEIN


From the University Health Network, University of Toronto, Toronto, Ontario, Canada.

Dr. O'Shea is the recipient of an unrestricted traveling fellowship from the Irish Society for Rheumatology and Wyeth Pharmaceuticals.

F.D. O'Shea, MB MRCPI, Division of Rheumatology, Toronto Western Hospital; F.W. Tsui, PhD, Department of Cell and Molecular Biology, Toronto Western Research Institute; B. Chiu, PhD, Toronto Western Research Institute; H.W. Tsui, PhD, Toronto Western Research Institute; M. Yazdanpanah, PhD, Division of Biochemistry, Toronto General Hospital; R.D. Inman, MD, Division of Rheumatology, Toronto Western Hospital, Department of Cell and Molecular Biology, Toronto Western Research Institute.

Address reprint requests to Dr. R.D. Inman, Arthritis Center of Excellence, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario M5T 2S8. E-mail: Robert.Inman @uhn.on.ca

Accepted for publication August 17, 2007.




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