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Selenium Deficiency and Toxicity
Selenium (Se) is a part of the enzyme glutathione peroxidase, which metabolizes hydroperoxides formed from polyunsaturated fatty acids. Selenium is also a part of the enzymes that deiodinate thyroid hormones. Generally, selenium acts as an antioxidant that works with vitamin E. Some epidemiologic studies associate low selenium levels with cancer. Plasma levels vary from 8 to 25 mcg/dL, depending on selenium intake.
Diagnosis of deficiency or toxicity is usually clinical; sometimes blood glutathione peroxidase is measured.
Selenium deficiency is rare, even in New Zealand and Finland, where selenium intake is 30 to 50 mcg/day, compared with 100 to 250 mcg/day in the US and Canada.
In certain areas of China, where intake averages 10 to 15 mcg/day, selenium deficiency predisposes patients to Keshan disease, an endemic viral cardiomyopathy affecting primarily children and young women. This cardiomyopathy can be prevented but not cured by sodium selenite supplements of 50 mcg/day po.
Patients receiving long-term TPN have developed selenium deficiency with muscle pain and tenderness that responded to a selenomethionine supplement.
In Siberian Russia and China, growing children with selenium deficiency may develop chronic osteoarthropathy (Kashin-Beck disease).
Selenium deficiency may contribute synergistically with iodine deficiency to the development of goiter and hypothyroidism.
Diagnosis of selenium deficiency is made clinically or sometimes by measuring glutathione peroxidase activity or plasma selenium, but neither of these tests is readily available.
Treatment of selenium deficiency consists of sodium selenite 100 mcg/day po.
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