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In patients with isolated selenium deficiency (such as patients with phenylketonuria receiving a low\u2010protein diet), peripheral thyroid hormone metabolism is impaired but there are no changes in thyrotropin (TSH) or clinical signs of hypothyroidism, suggesting that these patients are euthyroid. Selenium supplementation may be advisable to optimize tissue GPx activity and prevent potential oxidative stress damage. In areas where combined selenium and iodine deficiencies are present (such as endemic goiter areas in Central Africa), selenium deficiency may be responsible for the destruction of the thyroid gland in myxoedematous cretins but may also play a protective role by mitigating fetal hypothyroidism. In these areas, selenium supplementation should only be advocated at the same time or after iodine supplementation. In patients with absent or decreased production of thyroid hormones and who rely solely on deiodination of exogenous L\u2010thyroxine for generation of the active triiodothyronine (such as patients with congenital hypothyroidism), selenium supplementation may optimize thyroid hormone feedback at the pituitary level and decrease stimulation of the residual thyroid tissue.<\/jats:p>","DOI":"10.1002\/biof.5520190306","type":"journal-article","created":{"date-parts":[[2008,12,19]],"date-time":"2008-12-19T01:18:24Z","timestamp":1229649504000},"page":"137-143","source":"Crossref","is-referenced-by-count":26,"title":["Selenium and thyroid function in infants, children and 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