Detecting zinc deficiency
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Zinc is an essential element; it is a critical cofactor for carbonic anhydrase, alkaline phosphatase, RNA and DNA polymerases, alcohol dehydrogenase, and many other physiologically important proteins. The peptidases, kinases, and phosphorylases are most sensitive to zinc depletion. Zinc is a key element required for active wound healing.
Zinc depletion occurs either because it is not absorbed from the diet (excess copper or iron interfere with absorption) or it is lost after absorption. Dietary deficiency may be due to absence (parenteral nutrition) or because the zinc in the diet is bound to phytate (fiber) and not available for absorption. Excess copper and iron in the diet (eg, iron supplements) interfere with zinc uptake. Once absorbed, the most common route of loss is via exudates from open wounds or gastrointestinal loss. Zinc depletion occurs in burn patients who lose zinc in the exudates from their burn sites. Hepatic cirrhosis causes excess loss of zinc by enhancing renal excretion. Other diseases that cause low serum zinc are ulcerative colitis, Crohn's disease, regional enteritis, sprue, intestinal bypass, neoplastic disease, and increased catabolism induced by anabolic steroids. The conditions of anorexia and starvation also result in low zinc levels.
Zinc excess is not of major clinical concern. The popular American habit of taking megavitamins (containing huge doses of zinc) produces no direct toxicity problems. Much of this zinc passes through the gastrointestinal tract and is excreted in the feces. The excess fraction that is absorbed is excreted in the urine. The only known effect of excessive zinc ingestion relates to the fact that zinc interferes with copper absorption, which can lead to hypocupremia.
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.
0-10 years: 0.60-1.20 mcg/mL
> or =11 years: 0.66-1.10 mcg/mL
Normal serum zinc is 0.66 to 1.10 mcg/mL.
Burn patients with acrodermatitis may have zinc as low as 0.4 mcg/mL; these patients respond quickly to zinc supplementation.
Elevated serum zinc is of minimal clinical interest.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Hemolyzed specimens will cause false elevation of serum zinc levels.
It is essential that the specimen is collected following the trace metals collection procedure (see Trace Metals Analysis Specimen Collection and Transport in Special Instructions.)
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.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Tucker SB, Schroeter AL, Brown PW Jr, McCall JT: Acquired zinc deficiency: cutaneous manifestations typical of acrodermatitis enteropathica. JAMA 1976;235:2399-2402
2. Skelton JA, Havens PL, Werlin SL. Nutrient deficiencies in tube-fed children. Clin Pediatr 2006;45(1):37-41
3. Zorbas YG, Kakuris KK, Neofitov IA, Afoninos NI: Zinc utilization in zinc-supplemented and -unsupplemented healthy subjects during and after prolonged hypokinesis. Tr Elem Electro 2008;25:60-68