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Zinc Deficiency and Toxicity
Zinc (Zn) is contained mainly in bones, teeth, hair, skin, liver, muscle, leukocytes, and testes. Zinc is a component of several hundred enzymes, including many nicotinamide adenine dinucleotide (NADH) dehydrogenases, RNA and DNA polymerases, and DNA transcription factors as well as alkaline phosphatase, superoxide dismutase, and carbonic anhydrase.
A diet high in fiber and phytate (eg, in whole-grain bread) reduces zinc absorption.
Dietary deficiency is unlikely in healthy persons. Secondary zinc deficiency can develop in the following:
Some patients with hepatic insufficiency (because the ability to retain zinc is lost)
Patients taking diuretics
Patients with diabetes mellitus, sickle cell disease, chronic kidney disease, chronic alcoholism, or malabsorption
Patients with stressful conditions (eg, sepsis, burns, head injury)
Elderly institutionalized and homebound patients (common)
Maternal zinc deficiency may cause fetal malformations and low birth weight.
Zinc deficiency in children causes impaired growth and impaired taste (hypogeusia). Other symptoms and signs in children include delayed sexual maturation and hypogonadism. In children or adults, symptoms include hypogonadism, alopecia, impaired immunity, anorexia, dermatitis, night blindness, anemia, lethargy, and impaired wound healing.
Zinc deficiency should be suspected in undernourished patients with typical symptoms or signs. However, because many of the symptoms and signs are nonspecific, clinical diagnosis of mild zinc deficiency is difficult. Laboratory diagnosis is also difficult. Low albumin levels, common in zinc deficiency, make serum zinc levels difficult to interpret; diagnosis usually requires the combination of low levels of zinc in serum and increased urinary zinc excretion. If available, isotope studies can measure zinc status more accurately.
Treatment consists of elemental zinc 15 to 120 mg po once/day until symptoms and signs resolve.
Acrodermatitis enteropathica (a rare, once fatal autosomal recessive disorder) causes malabsorption of zinc. Psoriasiform dermatitis develops around the eyes, nose, and mouth; on the buttocks; and in an acral distribution. The disorder also causes hair loss, paronychia, impaired immunity, recurrent infection, impaired growth, and diarrhea. Symptoms and signs usually develop after infants are weaned from breast milk. In such cases, doctors suspect the diagnosis. If correct, zinc sulfate 30 to 150 mg/day po usually results in complete remission.
The recommended upper limit for zinc intake is 40 mg/day. Toxicity is rare.
Ingesting doses of elemental zinc ranging from 100 to 150 mg/day for prolonged periods interferes with copper metabolism and causes low blood copper levels, RBC microcytosis, neutropenia, and impaired immunity; higher doses should be given only for short periods of time and the patient followed closely.
Ingesting larger amounts (200 to 800 mg/day), usually by consuming acidic food or drink from a galvanized (zinc-coated) container, can cause anorexia, vomiting, and diarrhea. Chronic toxicity may result in copper deficiency and may cause nerve damage.
Metal fume fever, also called brass-founders’ ague or zinc shakes, is caused by inhaling industrial zinc oxide fumes; it results in fever, dyspnea, nausea, fatigue, and myalgias. Symptom onset is usually 4 to 12 h after exposure. Symptoms usually resolve after 12 to 24 h in a zinc-free environment.
Diagnosis of zinc toxicity is usually based on the time course and a history of exposure.
Treatment of zinc toxicity consists of eliminating exposure to zinc; no antidotes are available.
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