|Values are valid only on day of printing.|
Selenium is an essential element. It is a cofactor required to maintain glutathione peroxidase (GSH-Px) activity, an enzyme that catalyzes the degradation of organic hydroperoxides. The absence of selenium correlates with loss of GSH-Px activity and is associated with damage to cell membranes due to accumulation of free radicals.
In humans, cardiac muscle is the most susceptible to selenium deficiency. With cell membrane damage, normal cells are replaced by fibroblasts. This condition is known as cardiomyopathy and is characterized by an enlarged heart whose muscle is largely replaced by fibrous tissue.
In the United States, deficiency is related to use of total parenteral nutrition. This is therapy administered to patients with no functional bowel, such as after surgical removal of the small and large intestine because of cancer, or because of acute inflammatory bowel disease such as Crohn's disease. Selenium supplementation to raise serum concentration >90 ng/mL is the usual treatment. Serum monitoring done on a semi-annual basis checks the adequacy of supplementation.
Selenium toxicity has been observed in animals when daily intake exceeds 4 parts per million (ppm). Teratogenic effects are frequently noted in the offspring of animals living in regions where soil content is high in selenium such as south-central South Dakota and northern-coastal regions of California. Selenium toxicity in humans is not known to be a significant problem except in acute overdose cases. Selenium is not classified as a human teratogen.
Selenium is found in many over-the-counter vitamin preparations because its antioxidant activity is thought to be anticarcinogenic. There is no supporting evidence that selenium suppresses cancer.
Urine quantitation is used to assess clearance and in balance studies.
Monitoring selenium replacement therapy
The normal daily intake of selenium is 10 to 35 mcg/day, therefore, the usual daily output should be the same.
Daily excretion of <15 mcg/g creatinine indicates a lack of adequate selenium nutriture. Insufficient selenium intake leads to cardiomyopathy.
Selenium output of >40 mcg/g creatinine indicates excessive intake. There is no known toxicity to humans due to intake of modest excesses.
Grossly excessive intake (daily output >500 mcg/g creatinine) may have a teratogenic impact. This effect has been demonstrated in animals.
High concentrations of gadolinium, iodine and barium are known to interfere with most metals tests. If gadolinium-, iodine- or barium-containing contrast media has been administered, a specimen cannot be collected for 96 hours.
> or =16 years: 15-40 mcg/g creatinine
Reference values have not been established for patients who are <16 years of age.
1. Fleming CR, McCall JT, O'Brien JF, et al: Selenium status in patients receiving home parenteral nutrition. J Parenter Enteral Nutr 1984;8:258-262
2. Chariot P, Bignani O: Skeletal muscle disorders associated with selenium deficiency in humans. Muscle Nerve 2003 Jun;27(6):662-668
3. Kvicala J, Zamrazil V, Nemecek J, Anke M: Intake of selenium by seniors of South Bohemia and urine selenium of seniors in the course of a 1-year supplementation by various selenium species. Tr Element Electro 2008;25:21-24