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Ultraviolet radiation intensity predicts the relative distribution of dermatomyositis and anti–Mi-2 autoantibodies in women

✍ Scribed by Lori A. Love; Clarice R. Weinberg; D. Robert McConnaughey; Chester V. Oddis; Thomas A. Medsger Jr.; John D. Reveille; Frank C. Arnett; Ira N. Targoff; Frederick W. Miller


Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
71 KB
Volume
60
Category
Article
ISSN
0004-3591

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✦ Synopsis


Abstract

Objective

Because studies suggest that ultraviolet (UV) radiation modulates the myositis phenotype and Mi‐2 autoantigen expression, we conducted a retrospective investigation to determine whether UV radiation may influence the relative prevalence of dermatomyositis and anti–Mi‐2 autoantibodies in the US.

Methods

We assessed the relationship between surface UV radiation intensity in the state of residence at the time of onset with the relative prevalence of dermatomyositis and myositis autoantibodies in 380 patients with myositis from referral centers in the US. Myositis autoantibodies were detected by validated immunoprecipitation assays. Surface UV radiation intensity was estimated from UV Index data collected by the US National Weather Service.

Results

UV radiation intensity was associated with the relative proportion of patients with dermatomyositis (odds ratio [OR] 2.3, 95% confidence interval [95% CI] 0.9–5.8) and with the proportion of patients expressing anti–Mi‐2 autoantibodies (OR 6.0, 95% CI 1.1–34.1). Modeling of these data showed that these associations were confined to women (OR 3.8, 95% CI 1.3–11.0 and OR 17.3, 95% CI 1.8–162.4, respectively) and suggests that sex influences the effects of UV radiation on autoimmune disorders. Significant associations were not observed in men, nor were UV radiation levels related to the presence of antisynthetase or anti–signal recognition particle autoantibodies.

Conclusion

This first study of the distribution of myositis phenotypes and UV radiation exposure in the US showed that UV radiation may modulate the clinical and immunologic expression of autoimmune disease in women. Further investigation of the mechanisms by which these effects are produced may provide insights into pathogenesis and suggest therapeutic or preventative strategies.