Published in:
01-02-2013 | Editorial
Vitamin D deficiency in patients with Graves’ disease: probably something more than a casual association
Authors:
Mario Rotondi, Luca Chiovato
Published in:
Endocrine
|
Issue 1/2013
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Excerpt
In addition to its established role in calcium metabolism and skeletal homeostasis, vitamin D was recently identified as a factor playing a role in both innate and adaptive immunity (reviewed in Ref. [
1]). The vitamin D receptor is expressed on monocytes and activated lymphocytes and the biologically active metabolite of vitamin D, i.e., 1,25-dihydroxyvitamin D3 [1,25(OH)
2D
3], does modulate T cell responses [
1]. Studies in animal models of autoimmune diseases consistently showed that the administration of 1,25(OH)
2D
3 produces selective immunosuppressant effects, as assessed by its ability to either prevent or markedly suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes mellitus, and inflammatory bowel disease [
2]. Currently available clinical studies report a high prevalence of vitamin D deficiency in patients with several autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, type 1 diabetes mellitus, and Crohn’s disease [
3]. With specific regard to autoimmune thyroid diseases (AITD), available data remain controversial. The administration of 1,25(OH)
2D
3 had little effect in reducing the severity of experimental autoimmune thyroiditis induced by immunizing CBA mice with thyroglobulin [
4]. In a model of experimental Graves’ disease in which mice were immunized with adenovirus encoding for the TSH-receptor gene, BALB/cJ and C57BL/6J mice receiving either a sufficient or a deficient vitamin D diet developed comparable levels of TSH binding inhibitory and thyroid stimulating antibodies [
5]. The IgG subclasses of antibodies directed to the TSH-receptor were also similar in mice of either strain, irrespective of the treatment with a vitamin D-deficient or vitamin D-sufficient diet [
5]. However, as argued by the authors, it should be considered that in this experiment mice fed a vitamin D deficient diet, in spite of having nearly undetectable serum levels of 25(OH)D, displayed low but detectable concentrations of 1,25(OH)
2D. …