Affiliations: Department of Pediatrics, Endocrinology and Diabetes
Unit, University of British Columbia, Vancouver V6H 3V4, BC, Canada
Note: [] Address for correspondence: Jean-Pierre Chanoine, MD, Clinical
Professor and Head, Endocrinology and Diabetes Unit, Room K4-212, British
Columbia's Children's Hospital, 4480 Oak Street, Vancouver BC V6H 3V4, Canada.
Tel.: +1 604 875 2117; Fax: +1 604 875 3231; E-mail: jchanoine@cw.bc.ca
Abstract: Selenium is an integral component of the enzymes glutathione
peroxidase (GPx) and iodothyronine deiodinases. Although selenium nutrition
could conceivably affect thyroid function in infants, children and adolescents,
available data suggest that the effect of selenium deficiency on thyroid
function is relatively modest. In patients with isolated selenium deficiency
(such as patients with phenylketonuria receiving a low-protein 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-thyroxine 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.
