Clinical Information

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.