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Published in: Endocrine 1/2013

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)2D3], does modulate T cell responses [1]. Studies in animal models of autoimmune diseases consistently showed that the administration of 1,25(OH)2D3 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)2D3 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. …
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Metadata
Title
Vitamin D deficiency in patients with Graves’ disease: probably something more than a casual association
Authors
Mario Rotondi
Luca Chiovato
Publication date
01-02-2013
Publisher
Springer US
Published in
Endocrine / Issue 1/2013
Print ISSN: 1355-008X
Electronic ISSN: 1559-0100
DOI
https://doi.org/10.1007/s12020-012-9776-y

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