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Environmental factors and autoimmune thyroiditis

Abstract

Autoimmune thyroiditis, of which Hashimoto thyroiditis represents the most frequent form, is an inflammatory state of the thyroid gland that results from the interaction between genetic variants that promote susceptibility and environmental factors. High iodine intake, selenium deficiency, pollutants such as tobacco smoke, infectious diseases such as chronic hepatitis C, and certain drugs are implicated in the development of autoimmune thyroiditis, primarily in genetically predisposed people. Long-term iodine exposure leads to increased iodination of thyroglobulin, which increases its antigenicity and initiates the autoimmune process in genetically susceptible individuals. Selenium deficiency decreases the activity of selenoproteins, including glutathione peroxidases, which can lead to raised concentrations of hydrogen peroxide and thus promote inflammation and disease. Such environmental pollutants as smoke, polychlorinated biphenyls, solvents and metals have been implicated in the autoimmune process and inflammation. Environmental factors have not yet, however, been sufficiently investigated to clarify their roles in pathogenesis, and there is a need to assess their effects on development of the autoimmune process and the mechanisms of their interactions with susceptibility genes.

Key Points

  • Excess iodine intake is associated with a raised annual incidence of autoimmune thyroiditis in various parts of the world, probably owing to increased thyroglobulin antigenicity, although the exact mechanism is not yet fully understood

  • Selenium deficiency is thought to be involved in the pathogenesis of autoimmune thyroiditis and to lengthen its duration and exacerbate its severity; these effects may occur via reduced activity of the selenoprotein glutathione peroxidase, which leads to increased production of hydrogen peroxide

  • Environmental pollutants, such as polychlorinated biphenyls, metals and solvents, probably play a part in the development of autoimmune thyroiditis in genetically susceptible individuals, although research is urgently needed to clarify their precise roles

  • Inflammation induced by viral infections or by pollutants can modify cellular-signaling mediators and influence T-cell activity and cytokine-secretion profiles

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Figure 1: The evolution of autoimmune thyroiditis.

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Duntas, L. Environmental factors and autoimmune thyroiditis. Nat Rev Endocrinol 4, 454–460 (2008). https://doi.org/10.1038/ncpendmet0896

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