Two systematic review s have evaluated controlled trials among patients with autoimmune thyroiditis and report that selenium supplementation decreases circulating thyroid autoantibodies .
The immunomodulatory effects of selenium might involve reducing proinflammatory cytokine release .
In Graves ’ disease , some , but not all , trials indicate that adjuvant selenium supplementation enhances the restoration of biochemical euthyroidism , and might benefit patients with mild Graves ’ orbitopathy .
The available evidence from trials does not support routine selenium supplementation in the st and ard treatment of patients with autoimmune thyroiditis or Graves ’ disease .
However , correction of moderate to severe selenium deficiency may offer benefits in preventing , as well as treating , these disorders .
Purpose of review This review provides an appraisal of recent evidence for or against selenium supplementation in patients with autoimmune thyroid diseases , and discusses possible effect mechanisms .
Recent findings Epidemiological data suggest an increased prevalence of autoimmune thyroid diseases under conditions of low dietary selenium intake .
However , clinical ly relevant effects of selenium supplementation , including improvement in quality of life , are more elusive .
Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations.
In areas with severe selenium deficiency there is a higher incidence of thyroiditis due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells . Selenium-dependent enzymes also have several modifying effects on the immune system . Therefore , even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases . We performed a blinded , placebo-controlled , prospect i ve study in female patients ( n = 70 ; mean age , 47.5 + /- 0.7 yr ) with autoimmune thyroiditis and thyroid peroxidase antibodies ( TPOAb ) and /or Tg antibodies ( TgAb ) above 350 IU/ml . The primary end point of the study was the change in TPOAb concentrations . Secondary end points were changes in TgAb , TSH , and free thyroid hormone levels as well as ultrasound pattern of the thyroid and quality of life estimation . Patients were r and omized into 2 age- and antibody (TPOAb)-matched groups ; 36 patients received  200 microg ( 2.53 micromol ) sodium selenite/d , orally , for 3 months , and 34 patients  received placebo . All patients were substituted with L-T(4 ) to maintain TSH within the normal range . TPOAb , TgAb , TSH , and free thyroid hormones were determined by commercial assays . The echogenicity of the thyroid was monitored with high resolution ultrasound . The mean TPOAb concentration decreased significantly to 63.6 % ( P = 0.013 ) in the selenium group vs. 88 % ( P = 0.95 ) in the placebo group . A subgroup analysis of those patients with TPOAb greater than 1200 IU/ml revealed a mean 40 % reduction in the selenium-treated patients compared with a 10 % increase in TPOAb in the placebo group . TgAb concentrations were lower in the placebo group at the beginning of the study and significantly further decreased ( P = 0.018 ) , but were unchanged in the selenium group . Nine patients in the selenium-treated group had completely normalized antibody concentrations , in contrast to two patients in the placebo group ( by chi(2 ) test , P = 0.01 ) . Ultrasound of the thyroid showed normalized echogenicity in these patients . The mean TSH , free T(4 ) , and free T(3 ) levels were unchanged in both groups . We conclude that selenium substitution may improve the inflammatory activity in patients with autoimmune thyroiditis , especially in those with high activity . Whether this effect is specific for autoimmune thyroiditis or may also be effective in other endocrine autoimmune diseases has yet to be investigated
Two systematic review s have evaluated controlled trials among patients with autoimmune thyroiditis and report that selenium supplementation decreases circulating thyroid autoantibodies .
The immunomodulatory effects of selenium might involve reducing proinflammatory cytokine release .
In Graves ’ disease , some , but not all , trials indicate that adjuvant selenium supplementation enhances the restoration of biochemical euthyroidism , and might benefit patients with mild Graves ’ orbitopathy .
The available evidence from trials does not support routine selenium supplementation in the st and ard treatment of patients with autoimmune thyroiditis or Graves ’ disease .
However , correction of moderate to severe selenium deficiency may offer benefits in preventing , as well as treating , these disorders .
Purpose of review This review provides an appraisal of recent evidence for or against selenium supplementation in patients with autoimmune thyroid diseases , and discusses possible effect mechanisms .
Recent findings Epidemiological data suggest an increased prevalence of autoimmune thyroid diseases under conditions of low dietary selenium intake .
However , clinical ly relevant effects of selenium supplementation , including improvement in quality of life , are more elusive .