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Childrens Hospital Reine Fabiola (J.-P.C.), Laboratory of Pediatrics (P.B.), B 1020 Brussels, Belgium; Institute of Pharmacy (J.N.), B 1090 Brussels, Belgium; Centre Inter Universitaire Hôpital Ambroise Paré, Mons (J.V.), Free University of Brussels, B 7000 Brussels, Belgium; and Nuclear Medicine Medical Service (S.Y.W.), Veterans Affairs Medical Center, Long Beach, California 90822
Address all correspondence and requests for reprints to: Jean-Pierre Chanoine, M.D., Endocrinology and Diabetes Unit, British Columbias Childrens Hospital, 4480 Oak Street, Room 1A46, Vancouver V6H 3V4, Canada. E-mail: jchanoine{at}cw.bc.ca
Compared with euthyroid controls, patients with congenital hypothyroidism (CH) who are receiving L-T4 treatment show elevated serum TSH relative to serum T4 concentrations and increased T4/T3 ratio. These abnormalities could be the consequence of impaired activity of the selenoenzymes deiodinases on which patients with CH rely to convert the ingested L-T4 into active T3. Eighteen patients (0.515.4 yr), diagnosed with CH in infancy, received selenomethionine (SeM, 2060 µg selenium/day) for 3 months. The study took place in Belgium, a country where selenium intake is borderline. Compared with the values observed in age- and sex-matched euthyroid controls, patients with CH had decreased selenium, thyroglobulin and T3 concentrations and increased TSH, reverse T3, and T4 concentrations and T4/T3 ratio at baseline. Selenium supplementation caused a 74% increase in plasma selenium values but did not affect the activity of the selenoenzyme glutathione peroxidase used as a marker of selenium status. SeM abolished the TSH difference observed between CH patients and euthyroid controls at baseline and caused a significant decrease in thyroglobulin values. Thyroid hormone concentrations were not affected by SeM. In conclusion, our data suggest that selenium is not a limiting factor for peripheral T4-to-T3 conversion in CH patients. In contrast, we find indirect evidence that SeM improves thyroid hormones feedback at the hypothalamo-pituitary level and decreases stimulation of the residual thyroid tissue, possibly suggesting greater intracellular T4-to-T3 conversion.
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