Zinc, Serum

CPT CODE:

  • 84630

USEFUL FOR:

Detecting zinc deficiency

SPECIMEN REQUIRED:

1.  Draw blood in a plain, royal blue-top Monoject trace element     blood collection tube(s) - product #8881-307006 (Supply T184). 2.  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.3.  Remove the stopper. Carefully pour 0.4 mL of serum into a     7-mL Mayo metal-free, screw-capped, polypropylene vial     (Supply 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. 4.  See "Metals Analysis - Collection and Transport" in Special     Instructions for complete instructions.5.  Send specimen refrigerated.

TRANSPORT TEMPERATURE:

Refrig\Frozen OK\Ambient OK

CLINICAL INFORMATION:

Zinc is an essential element; it is a critical co-factor for carbonicanhydrase, 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 dietor 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. Once absorbed, the most common route of loss is via exudates from open wounds such as third degree burn or gastrointestinal loss as in colitis.Hepatic cirrhosis causes excess loss of zinc by enhancing renalexcretion. Zinc depletion occurs in burn patients who loose zinc in the exudates from their burn sites.
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 that can lead to hypocupremia.

CLINICAL INTERPRETATION:

Normal serum zinc is 0.66 mgc/mL to 1.10 mcg/mL.
Burn patients with acrodermatiitis may have zinc as low as 0.4 mcg/mL;these patients respond quickly to zinc supplementation.
Other diseases that cause low serum zinc are hepatic cirrhosis,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.
Elevated serum zinc is of minimal clinical interest.

REFERENCE VALUES:

0-10 years: 0.60-1.20 mcg/mL

> or =11 years: 0.66-1.10 mcg/mL

 

NIH UNITS

0-10 years: 60-120 mcg/dL

> or =11 years: 66-110 mcg/dL