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#Allergy and Immunology
Breast milk is the most ideal nutrient mix for infants till the age of 6 months. But, in certain cases, because of genetic modifications along with nutrient deficiencies in nursing mothers, infants might suffer from inadequate levels of micronutrients even in exclusive breastfeeding. As a result, transient neonatal zinc deficiency (TNZD) is caused due to loss-of-function mutations in the zinc transporter SLC30A2/ZnT2 gene, hence ensuing in poor secretion of zinc into the breast milk.
Subsequently, infants who are exclusively breastfed with zinc-deficient breast milk can develop severe zinc deficiency. The foremost primary symptoms of zinc deficiency are dermatitis, alopecia diarrhea and loss of appetite. Notably, supplementation of zinc in these zinc-deficient infants can rapidly and effectively resolve these TNZD symptoms. In this review article, the major phases of the identification of the molecular mechanisms underlying TNZD are presented and also novel methods that could be implemented to achieve an early diagnosis of TNZD in the prevention of TNZD morbidity are proposed. The importance of evaluating the incidence of TNZD in the general population is also discussed, while taking consideration of its autosomal dominant inheritance.
Evidence indicate that TNZD is more common than primarily assumed. Increasing number of TNZD cases have been reported of late. All of this emphasizes the importance of early diagnosis of SLC30A2/ZnT2 variants to supplement zinc-deficient infants in actual, hence preventing TNZD morbidity and improving new-born health. The early genetic diagnosis of zinc deficiency can possibly be a useful platform for the identification of other micronutrient deficiencies that can be readily resolved by appropriate real-time supplementation of the infants diet.
Source: Golan Y, Kambe T, Assaraf YG. The role of the zinc transporter SLC30A2/ZnT2 in transient neonatal zinc deficiency. Metallomics. 2017;9(10):1352-1366. doi:10.1039/c7mt00162b