Transient symptomatic zinc deficiency
Transient symptomatic zinc deficiency
Description, Causes and Risk Factors:
Zinc is an essential trace element required by all living organisms because of its critical roles both as a structural component of proteins and as a cofactor in enzyme catalysis. The importance of zinc in human metabolism is illustrated by the effects of zinc deficiency, which include a diminished immune response, reduced healing and neurological disorders. Furthermore, nutritional zinc deficiency can be fatal in newborn or growing animals. Zinc affects T- and B-lymphocytes, depresses baseline and antibody-dependent cytotoxic activity of killer lymphocytes, and phagocytic and bactericidal capacities of neutrophils.
Serum zinc concentrations do not necessarily re?ect body zinc content, and ?uctuate widely depending on nutrition, time of sampling, stress, infection or other causes of cytokine release, and albumin concentration. Decreasing alkaline phosphatase, often welcomed by the clinician as a sign of improving osteopenia of prematurity, may signal subclinical zinc de?ciency.
The zinc deficiency is commonly caused by dietary factors, several inherited defects of zinc deficiency have been identified. Acrodermatitis enteropathica is the most commonly described inherited condition found in humans. In several of the few cases that have been reported, this disorder is associated with mutations in the hZIP4 gene, a member of the SLC39 family, whose members encode membrane-bound putative zinc transporters. Mutations in other members of this family or in different genes may account for other cases of acrodermatitis in which defects in hZIP4 have not been detected.
Another inherited form of zinc deficiency occurs in the lethal milk mouse, where a mutation in ZnT4 gene, a member of the SLC30 family of transmembrane proteins results in impaired secretion of zinc into milk from the mammary gland. A similar disorder to the lethal milk mouse occurs in humans. In the few cases studied, no changes in ZnT4 orthologue, hZnT4, were detected. This, and the presence of several minor phenotypic differences between the zinc deficiency in humans and mice, suggests that the human condition is caused by defects in genes that are yet to be identified.
Taking into account the fact that there are no definitive tests for zinc deficiency and that this disorder can go undiagnosed, plus the recent identification of multiple members of the SCL30 and SLC39, it is likely that mutations in other genes may underlie additional inherited disorders of zinc deficiency.
While dietary factors that reduce the availability of zinc are the most common cause of zinc deficiency, inherited defects can also result in zinc deficiency. Both nutritional and inherited zinc deficiency produce similar symptoms. An outstanding feature of zinc deficiency is the broad range of pathologies produced. This is not surprising considering the number of physiological processes for which zinc is required and that over 300 mammalian enzymes are zinc-dependant.
The initial effects ofzinc deficiency include dermatitis, diarrhea, alopecia and loss ofappetite. More prolonged deficiencyresults in growth impairment and neuropsychological changessuch as emotional instability, irritability and depression.Immune disorders and susceptibility to infections, iron deficiency anemia, macular degeneration, night blindness, impaired taste and smell, impaired wound healing.
Hypoproteinemia spuriously lowers the measured plasma zinc concentration.
Reduced alkaline phosphatase and plasma testosterone.
Impaired T-lymphocyte function.
Decreased collagen synthesis (resulting in poor wound healing), and decreased RNA polymerase activity in several tissues.
Diagnosis may be difficult to confirm, particularly with mild levels of deficiency. Decreased levels of plasma zinc (less than 10.7 ?mol/L). Plasma levels are an unreliable indicator of zinc deficiency because the plasma level may be lowered, e.g. in acute infection and after trauma.
Dietary advice and zinc supplementation if necessary.
Zinc supplementation has a positive effect on growth in premature infants.
There is weak evidence that zinc supplementation may help to heal leg ulcers in patients with low serum zinc.
Management is based on both treatment of any underlying cause and zinc supplementation. Zinc deficiency often coexists with other micronutrient deficiencies including iron, making single supplements inappropriate.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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