26626 Zinc, Serum (ZN_S)

​Zn (Zinc) Serum

​Detecting zinc deficiency

​Patient Preparation: High concentrations of gadolinium, iodine, and barium are known to interfere with most metal tests. If gadolinium-, iodine, or barium-containing contrast media has been administered, the specimen should not be collected for 96 hours.​

1. This specimen must always be drawn first.
2. Do not collect specimen from a line.
3. Allow the specimen to clot for 30 minutes; then centrifuge the specimen to separate serum from the cellular fraction. Serum must be removed from cellular fraction within 4 hours of specimen collection. Avoid hemolysis.
4. Remove the stopper. Carefully pour specimen into a Mayo metal-free, polypropylene vial (T173), avoiding transfer of the cellular components of blood. Do not insert a pipet into the serum to accomplish transfer, and do not ream the specimen with a wooden stick to assist with serum transfer.

Gross hemolysis

​Hemolyzed specimens will cause false elevation of serum zinc levels.

Specimens collected through a vascular line may falsely increase the zinc level. Consider recollection by venipuncture if clinically indicated.

It is essential that the specimen is collected following the trace metals collection procedure, see Metals Analysis Specimen Collection and Transport on Mayo Lab's website.

​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 because it is either not absorbed from the diet (excess copper or iron interfere with absorption) or 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 kidney excretion. Other diseases that cause low serum zinc are ulcerative colitis, Crohn 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 mega-vitamins (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.

​Normal serum zinc levels are from 66 to 106 mcg/dL in adults.

Burn patients with acrodermatitis may have zinc levels as low as 40 mcg/dL; these patients respond quickly to zinc supplementation.

An elevated serum zinc concentration is of minimal clinical interest.