Zinc is an integral part of numerous enzymes associated with carbohydrate and energy metabolism, protein synthesis and degradation, nucleic acid synthesis, intercellular transport functions and protection from oxidative damage.
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Its effects, however, are most obviously seen in the maintenance of skin integrity and in wound healing. It plays a role in maintaining exocrine and endocrine pancreatic function. Spermatogenesis is also a zinc-dependent process based on the metal's role in testosterone metabolism.
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Absorption of zinc from the diet is an active process and shares gut transport mechanisms with copper and iron
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On absorption, zinc is found bound to the protein metallothioneine, a cysteine-rich protein, which is also associated with the binding of other divalent metal ions such as copper. Its synthesis is dependent on the amount of trace metals present in the diet. Its excess may interfere with copper absorption. Zinc is probably the least toxic of the trace metals but increased oral doses of zinc interfere with copper absorption leading to deficiency of the latter.
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Zinc deficiency affects growth, skin integrity and wound healing
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Zinc deficiency is not uncommon: in children it is characterized by growth retardation, skin lesions, and impairment of sexual development. A specific inherited defect in the absorption of zinc from the gut was identified in the 1970s; it was termed acrodermatitis enteropathica with the clinical appearance of severe skin lesions, diarrhea, and loss of hair (alopecia). Its deficiency also leads to impairment in taste and smell and to delayed wound healing.
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Increased losses of zinc occur in patients with major burns and in those with renal damage. Zinc loss in renal disease is due to its association with plasma albumin, and it accompanies urinary protein loss. Substantial amounts of zinc may be also lost during dialysis. Increased metallothioneine synthesis is part of the metabolic response to trauma and results in a reduction of serum zinc concentration. During intravenous feeding, in situations where there is frequently an increased demand, failure to replace it may produce a symptomatic deficiency.
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Measurement of serum zinc concentration is the usual method of assessing zinc status. However, many conditions and environmental factors can affect its concentration in plasma, including inflammation, stress, cancer, smoking, steroid administration and hemolysis. More recently, erythrocyte metallothioneine levels have proved more appropriate in assessing zinc status.
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A 34-year-old man who required total intravenous feeding had been receiving the same prescription for some 4 months, with no assessment of his trace metal status. During this time, he continued to have major gastrointestinal losses and intermittent pyrexia. Initially, he developed a rash across his face, head, and neck, with accompanying hair loss and, by the end of the 4-month period, was clearly zinc-deficient. He had a widespread acne-type rash and was virtually devoid of hair. His serum zinc concentration at that time was less than 1 μmol/L (range: 9-20 μmol/L; 60-130 μg/dL). |
Comment. Patients with major catabolic illness and increased gastrointestinal losses have markedly increased zinc requirements. The zinc-depleted state the patient developed would aggravate his illness: (a) by preventing healing of his gastrointestinal lesions; and (b) by making him more susceptible to infection due to defects in his immune competence. Patients receiving intravenous feeding need to have their micronutrient status checked regularly and prescriptions altered if required. |
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