Zinc-deficiency dermatitis in breast-fed infants

Kienast, Antonia K.; Roth, Bernhard; Bossier, Christiane; Hojabri, Christina; Hoeger, Peter H.

doi:10.1007/s00431-006-0218-9

Cited by 28 publications

(18 citation statements)

References 27 publications

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“…Symptomatic zinc deficiency has been reported in infants. Most reported cases are breast-fed preterm infants [7]–[10], because the zinc concentration in human milk is much lower than that of cow's milk, and the demand for zinc increases rapidly in thriving preterm infants [11]. Zinc deficiency may also occur in breast-fed full-term infants, although it is rare [1]–[17].…”

Section: Introductionmentioning

confidence: 99%

Compound Heterozygous Mutations in SLC30A2/ZnT2 Results in Low Milk Zinc Concentrations: A Novel Mechanism for Zinc Deficiency in a Breast-Fed Infant

et al. 2013

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Zinc concentrations in breast milk are considerably higher than those of the maternal serum, to meet the infant's requirements for normal growth and development. Thus, effective mechanisms ensuring secretion of large amounts of zinc into the milk operate in mammary epithelial cells during lactation. ZnT2 was recently found to play an essential role in the secretion of zinc into milk. Heterozygous mutations of human ZnT2 (hZnT2), including H54R and G87R, in mothers result in low (>75% reduction) secretion of zinc into the breast milk, and infants fed on the milk develop transient neonatal zinc deficiency. We identified two novel missense mutations in the SLC30A2/ZnT2 gene in a Japanese mother with low milk zinc concentrations (>90% reduction) whose infant developed severe zinc deficiency; a T to C transition (c.454T>C) at exon 4, which substitutes a tryptophan residue with an arginine residue (W152R), and a C to T transition (c.887C>T) at exon 7, which substitutes a serine residue with a leucine residue (S296L). Biochemical characterization using zinc-sensitive DT40 cells indicated that the W152R mutation abolished the abilities to transport zinc and to form a dimer complex, indicating a loss-of-function mutation. The S296L mutation retained both abilities but was extremely destabilized. The two mutations were found on different alleles, indicating that the genotype of the mother with low milk zinc was compound heterozygous. These results show novel compound heterozygous mutations in the SLC30A2/ZnT2 gene causing zinc deficiency in a breast-fed infant.

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Section: Introductionmentioning

confidence: 99%

Compound Heterozygous Mutations in SLC30A2/ZnT2 Results in Low Milk Zinc Concentrations: A Novel Mechanism for Zinc Deficiency in a Breast-Fed Infant

et al. 2013

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“…Signs of deficiency include growth impairment (linear and ponderal), characteristic dermatitis similar to that described above for AE, and moderately low plasma/serum zinc concentrations [20,25,26,27]. In one large series from a hospital population, the strongest clinical risk factors include low gestational age, small for gestational age (SGA), and intestinal resection [28].…”

Section: Acquired Zinc Deficiencymentioning

confidence: 99%

Update on Zinc Deficiency and Excess in Clinical Pediatric Practice

Krebs¹

2013

Ann Nutr Metab

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The critical importance of adequate zinc status to human health, including normal growth and development, is indisputable. The high prevalence of zinc deficiency on a global basis and its importance to public health have been well documented through large-scale randomized controlled zinc supplementation trials. Similar evidence in the clinical setting, however, is much less widely available due to the nonspecific features of zinc deficiency and to the lack of sensitive biomarkers to detect zinc deficiency, especially that of a mild degree of severity. The current understanding of zinc homeostasis indicates that the primary determinants of zinc absorption are the amount of zinc ingested and dietary phytate, the latter having a major effect on zinc bioavailability. In normal as well as in many pathologic conditions, the gastrointestinal tract is the major site of zinc losses resulting from secretion of endogenous zinc into the lumen and subsequent excretion in the feces. The amount excreted is dependent on host status, the amount reabsorbed, and sometimes the presence of pathophysiologic conditions, including diarrhea and steatorrhea. Assessment in the clinical setting dictates that the clinician obtain a careful medical and diet history, recognize clinical presentations in which zinc adequacy may be compromised, and link this risk with nonspecific but plausible manifestations of deficiency. Examples discussed in this article include primary zinc deficiency due to dietary inadequacy (older breastfed infants or toddlers without zinc-rich complementary foods); genetically based deficiency (acrodermatitis enteropathica, acquired zinc deficiency of lactogenic origin), and acquired secondary deficiency in low birth weight and prematurity, gastrointestinal and hepatic disease, and cystic fibrosis. Evidence for efficacy of zinc therapy with pharmacologic doses for two conditions, Wilson's disease and viral upper respiratory infections, is also discussed.

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“…Breast milk zinc concentrations, particularly in the first 3 mo, are considerably higher than those of the maternal serum, which reflects the infant's requirement of a large amount of zinc for growth and development. Compared with full-term infants, preterm infants are in negative zinc balance at birth because of the lower capacity for gut absorption (6), and thus the demand for zinc increases rapidly in thriving preterm infants (7). Hence, the preterm infant has an increased risk of zinc deficiency and symptomatic zinc deficiency has been mostly found in breast-fed preterm infants (8).…”

Section: Requirement Of Zinc For Optimal Growth Of Infants and Childrenmentioning

confidence: 99%