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There have been two main forms of AE identified that are clinically distinguishable from each other. The first form of the disorder is an acquired form resulting from a dietary zinc deficiency that resolves upon zinc repletion. The other form is an inheritable disease caused by a mutation in the SLC39A4 gene, which codes for the hZip4 Zn transporter protein, and it is inherited in an autosomal recessive pattern. One or more of its symptoms are often observed in the later stages of the disorder [1].
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This page is a summary of: Analysis of Disorder, January 2015, Springer Science + Business Media,
DOI: 10.1007/978-3-319-17819-6_3.
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