Most of the previously reported cases in premature and also full-

Most of the previously reported cases in premature and also full-term infants were associated with low zinc levels in the maternal milk, although in some cases maternal zinc level

was normal. A low zinc level in the maternal milk is an important cofactor. Breast milk may be low in zinc because of a rare abnormality of zinc secretion by the mammary normally gland [16]. This may be the cause of symptomatic zinc deficiency, which is more severe and more common in premature infants because of the increased zinc requirements in this group. Symptomatic zinc deficiency can also appear from a combination of the SLC39A4 mutation in the infant and low milk zinc concentration from the mother who has the same heterozygous mutation [2].

All our patients had an excellent clinical improvement and discontinued the treatment after 2-3 months with no relapses. This indicates the diagnosis of TNZD and made us exclude AE, which requires lifelong treatment. Breast feeding, partial or total, was also a supporting factor for the diagnosis. Zinc deficiency may also be secondary to a poor intestinal absorption or an increased urinary and intestinal secretion [13]. Disorders of intestinal malabsorption are other possible etiologic factors. None of the children reported here had clinical evidence of intestinal disease. It was not possible to measure urinary zinc levels. In our patients, we were not able to demonstrate any increased demand for zinc or any decreased ability of zinc storage. In fact, none of them was evidently preterm, had burns, had parenteral nutrition, or had any other evident reason to require increased zinc supplementation. We could not rule out whether mother and child presented heterozygosity

for a SLC39A4 or SLC30A2 gene mutation or whether the clinical features could be due to a dietary zinc deficiency of the mothers and/or increased zinc requirements of the infants. All the mothers were asymptomatic and had no skin abnormalities. As reported in previous studies from different regions of Ethiopia [17–19], they could also probably have a primary dietary asymptomatic zinc deficiency. Since sophisticated diagnostic techniques are not generally available in developing countries, our diagnosis was clinical and confirmed by the prompt and remarkable healing of the lesions after treatment with oral zinc supplement. Most GSK-3 probably, an association of both heterozygosity for SLC30A2 gene mutation and dietary zinc deficiency in the mothers was contributing to the clinical manifestations in the infants. Zinc is essential for growth, as it is involved in the development of the immune system, the muscles, and the bones, as well as the skin. In developing countries, diets often do not contain zinc in sufficient quantity or of sufficient bioavailability [18, 19].

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