Interpretive Handbook

Test 60077 :
Selenium, Random, Urine

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

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.

Useful For Suggests clinical disorders or settings where the test may be helpful

Monitoring selenium replacement therapy

Interpretation Provides information to assist in interpretation of the test results

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/L indicates a lack of adequate selenium nutriture. Insufficient selenium intake leads to cardiomyopathy.


Selenium output of >50 mcg/L indicates excessive intake. There is no known toxicity to humans due to intake of modest excesses.


Grossly excessive intake (daily output >500 mcg/L) may have a teratogenic impact. This effect has been demonstrated in animals.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

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 should not be collected for 96 hours.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

0-15 years: not established

> or =16 years: 15-50 mcg/L

Clinical References Provides recommendations for further in-depth reading of a clinical nature

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, et al: 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. Trace Elements and Electrolytes 2008;25:21-24