selenium

Selenium is incorporated into selenoproteins as selenocysteine, the 21st amino acid, via a unique tRNA-mediated cotranslational mechanism. Key selenoenzymes include glutathione peroxidase (reduces H2O2 and lipid peroxides, protecting cell membranes from oxidative stress), thioredoxin reductase (maintains redox balance, supports DNA synthesis), and iodothyronine deiodinases (convert T4 to active T3, critical for thyroid hormone regulation).

Deficiency states: Selenium deficiency is classically associated with Keshan disease, an endemic dilated cardiomyopathy first described in Keshan, China, linked to low soil selenium content, often exacerbated by coxsackievirus B infection. Kashin-Beck disease is a deforming osteoarthropathy also linked to selenium deficiency, seen in similar geographic regions. Deficiency can also occur in patients on long-term total parenteral nutrition (TPN) without adequate supplementation, leading to cardiomyopathy, skeletal muscle weakness, and macrocytosis. Deficiency also impairs thyroid hormone conversion, potentially worsening hypothyroidism, and can accentuate the effects of vitamin E deficiency since both are involved in antioxidant defense.

Toxicity: Selenosis (selenium toxicity) presents with garlic breath odor, hair and nail loss/brittleness, GI distress, irritability, and peripheral neuropathy. Chronic industrial or dietary overexposure can cause these symptoms.

Clinical relevance for boards: Know the link between selenium deficiency and Keshan/Kashin-Beck disease, its role as a glutathione peroxidase cofactor for antioxidant defense, its function in thyroid hormone metabolism, and the classic toxicity presentation (garlic breath, hair/nail changes). Selenium deficiency is also a boards-relevant consideration in patients with malabsorption syndromes or those on prolonged TPN.