Retinol (vitamin A) and retinol-binding protein levels are decreased in ankylosing spondylitis: clinical and genetic analysis

• Published in: Journal of rheumatology Vol. 34; no. 12; pp. 2457 - 2459
• Main Authors: O'SHEA, Finbar D, TSUI, Florence W. L, BASIL CHIU, HING WO TSUI, YAZDANPANAH, Mehrdad, INMAN, Robert D
• Format: Journal Article
• Language: English
• Published: Toronto, ON The Journal of Rheumatology 01-12-2007; Journal of Rheumatology Publishing
• Subjects: Adult; Aged; Biological and medical sciences; Case-Control Studies; Cytochrome P-450 Enzyme System - genetics; Diseases of the osteoarticular system; Diseases of the spine; Enzyme-Linked Immunosorbent Assay; Female; Humans; Inflammatory joint diseases; Male; Mass Spectrometry; Medical sciences; Middle Aged; Polymorphism, Single Nucleotide; Retinoic Acid 4-Hydroxylase; Retinol-Binding Proteins, Plasma - analysis; Retinol-Binding Proteins, Plasma - genetics; Spondylitis, Ankylosing - blood; Spondylitis, Ankylosing - genetics; Vitamin A - blood; Vitamin A - genetics; Human; GENETIC STUDIES; Activity index; DISEASE ACTIVITY; Diseases of the osteoarticular system; Vitamin; Exploration; Inflammatory joint disease; RETINOL BINDING PROTEIN; Spine disease; Retinol; Spondylarthropathy; Binding protein; Chronic; Ankylosing hyperostosis; Treatment; Genetics; Bone; Single nucleotide polymorphism; Mass spectrometry; ELISA assay; Ankylosing spondylitis
• ISSN: 0315-162X; 1499-2752

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 micromol/l for AS, 3.34 +/- 1.01 micromol/l
for controls; p < 0.0001). Retinol-binding protein levels were also lower in AS than controls (AS 4.65 +/- 2.10 microg/l;
controls 7.48 +/- 4.87 microg/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.