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Article: Roberto Negro, Gabriele Greco, Tiziana Mangieri, Antonio Pezzarossa, Davide Dazzi, and Haslinda Hassan The Influence of Selenium Supplementation on Postpartum Thyroid Status in Pregnant Women with Thyroid Peroxidase Autoantibodies J Clin Endocrinol Metab 2007; 0: jc.2006-1821v1 [Abstract]

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Selenium Treatment in Autoimmune Thyroiditis. Why do We Need High Dose?

Omer Turker, Ismail Dogan.   (7 March 2007)

Selenium Treatment in Autoimmune Thyroiditis. Why do We Need High Dose? 7 March 2007
Omer Turker, Nuc. Med. Akademi T.M., Ismail Dogan. Send letter to journal: Re: Selenium Treatment in Autoimmune Thyroiditis. Why do We Need High Dose? otturker{at}yahoo.com Omer Turker, et al.	In their interesting study, Negro et al. speculate that “TPOAb reduction (by selenium) is dose-dependent and requires doses higher than 100 μg/d to maximize glutathione peroxidase (GPX) activity” (1). We disagree with their dose-response conclusions. Two hundred micrograms L-selenomethionine per day suppresses autoimmune activity, while lower doses fail (2). However, doses higher than 100 μg/d are not required to maximize GPX activity. This is a critical point, not with regard to the optimal daily selenium requirement, but to understand the effect of selenium on autoimmunity. The current recommended dietary intake of selenium to achieve the maximal activity of GPX in plasma or erythrocytes is between 55 and 75 μg/d (3). In another study, also for adults with low serum selenium levels, an upper estimated of 90 μg/d is calculated as the intake necessary for maximization of plasma GPX activity, as used to derive of the U.S. recommended daily allowance (4). An even lower intake of 39 μg/d is needed to reach two-thirds of maximal GPX activity, as was used in calculating the World Health Organization normative requirement (5). Our own study pointed out that the anti-TPO suppressive dose of selenium is higher than the dose needed to replenish deficient GPX stores (2). Furthermore, the lowering of serum TPOAb levels in patients whose GPX stores are saturated suggests that non-selenium-deficient autoimmune thyroiditis (AIT) patients may respond to a higher dose (200 µg/d) (2). Interestingly, in all of the clinical studies of Gartner, Duntas and these investigators, serum selenium levels of patients were within or close to the lower limit of the normal range (70–125 μg/l), but patients still responded to Se therapy. Consequently, it appears that maximization of GPX activity is not the main mechanism of action of selenium therapy. It is possible that there could be any altered selenium-binding capability of proteins in AIT patients. We need more data related to molecular biology of selenoproteins and the effects of these proteins on immune cells. These efforts may help us to understand the effects of selenium in other autoimmune diseases like asthma and rheumatoid arthritis. References 1. Negro R, Greco G, Mangieri T, Pezzarossa A, Dazzi D, Hassan H. 2007. The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. J Clin Endocrinol Metab (doi:10.1210/jc.2006-1821) 2. Turker O, Kumanlioglu K, Karapolat I, Dogan I. 2006. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. J Endocrinol 190:151–156 3. Rayman MP. 2000. The importance of selenium to human health. Lancet 356:233–241 4. Duffield AJ, Thomson CD, Hill KE, Williams S. 1999. An estimation of selenium requirements for New Zealanders. Am J Clin Nutr 70:896–903 5. Levander OA. 1997. Selenium requirements as discussed in the 1996 joint FAO/IAEA/WHO expert consultation on trace elements in human nutrition. Biomed Environ Sci 10:214–219