Selenium

Selenium is present at the active site of the enzymes glutathione peroxidase and type I iodo-thyronine 5’-deiodinase and is, therefore, involved in cellular antioxidant activity and conversion of T4 to T3. Selenium deficiency has been found to be endemic in parts of China leading to two recognisable diseases; Keshan syndrome (cardiomyopathy) and Kashin-Beck disease (osteoarthropathy in children). Selenium supplementation has been successful in virtually eradicating Keshan syndrome, but has only partly solved the problem of Kashin-Beck disease. Outside China, symptomatic selenium deficiency in humans appears to be restricted to patients on parenteral nutrition and children with inborn errors of metabolism on specialised diets.

Selenium is used in the electronics industry and in the manufacture of shampoos, paints, dyes and glass. Acute symptoms of toxicity include intense irritation of eyes, nose, mouth and lungs, chronic exposure producing, in addition, “garlic breath”, nausea and anorexia. Self-poisoning, accidental and deliberate, has occurred by ingestion of gun-blueing compound. There is some debate as to what is the most appropriate index of selenium status, but in clinical practice serum/plasma selenium is usually measured. Normal plasma selenium concentrations are age-dependent being lower in neonates. There is evidence that selenium is a negative acute phase reactant and this should be excluded by concurrent measurement of CRP.