Symptomatic zinc deficiency in breast‐fed term and premature infants

Stevens, Jennifer E.; Lubitz, Lionel

doi:10.1046/j.1440-1754.1998.00164.x

Cited by 69 publications

(35 citation statements)

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“…There is literature on manifest zinc deficiency in LBW infants [16,17,18], but none of our infants had any clinical signs that could suggest zinc deficiency. National level programs have been suggested in places with a prevalence of low serum zinc values exceeding 20% [7], but current guidelines do not recommend routine zinc supplementation even to LBW infants, presumably at higher risk.…”

Section: Discussionmentioning

confidence: 72%

Poor Zinc Status in Early Infancy among Both Low and Normal Birth Weight Infants and Their Mothers in Delhi

Agarwal

Virmani²,

Jaipal³

et al. 2012

Neonatology

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Background: Low birth weight (LBW) infants are at high risk of zinc deficiency, but there is a paucity of data on their zinc status. Objective: To evaluate zinc status of LBW (BW <2,500 g) and normal birth weight (NBW; BW ≥2,500 g) infants at birth and in early infancy. Methods: A total of 339 infants (LBW, n = 220; NBW, n = 119) were enrolled, and venous blood samples of mother-infant dyad were taken within 48 h of birth. Infants’ levels were repeated between 2 and 10 months of age. Serum zinc levels were estimated using an inductively coupled plasma mass spectrometer. Primary outcome was zinc deficiency, defined as serum zinc <65 µg/dl. Results: Zinc results were available for 182 LBW and 103 NBW infants at birth and for 100 LBW and 66 NBW infants at follow-up with a median postnatal age of 14 and 15.5 weeks, respectively. Median zinc levels were low and comparable at birth as well as at follow-up, with zinc deficiency being present in 51.0% of LBW and 42.4% of NBW infants at birth and in 79.0% of LBW and 66.7% of NBW infants at follow-up. Zinc levels decreased significantly in both groups from birth to follow-up, irrespective of zinc multivitamin supplementation. Zinc levels of infants with BW <2,000 g at follow-up were significantly lower compared to infants with higher BW. Conclusion: Zinc status was poor in many infants at birth irrespective of BW. Zinc status worsened significantly during early infancy, with infants with BW <2,000 g having the lowest zinc levels.

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Section: Discussionmentioning

confidence: 72%

Poor Zinc Status in Early Infancy among Both Low and Normal Birth Weight Infants and Their Mothers in Delhi

Agarwal

Virmani²,

Jaipal³

et al. 2012

Neonatology

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“…This condition has been reported in pre-term babies (27-33 weeks' gestation) (Aggett et al 1980;Connors et al 1983;Glover and Atherton 1988;Heinen et al 1995;Parker et al 1982;Stevens and Lubitz 1998;Weymouth et al 1982;Zimmerman et al 1982) and less commonly in term babies (Bye et al 1985;Khoshoo et al 1992;Stevens and Lubitz 1998). Prematurity does not explain the zinc deficiency despite higher requirements of pre-term babies for zinc; however, prematurity may affect predisposition to zinc deficiency.…”

Section: Introductionmentioning

confidence: 94%

Analysis of zinc transporter, hZnT4 ( Slc30A4 ), gene expression in a mammary gland disorder leading to reduced zinc secretion into milk

et al. 2003

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Zinc deficiency, causing impaired growth and development, may have a nutritional or genetic basis. We investigated two cases of inherited zinc deficiency found in breast-fed neonates, caused by low levels of zinc in the maternal milk. This condition is different from acrodermatitis enteropathica but has similarities to the "lethal milk" mouse, where low levels of zinc in the milk of lactating dams leads to zinc deficiency in pups. The mouse disorder has been attributed to a defect in the ZnT4 gene. Little is known about the expression of the human orthologue, hZnT4 (Slc30A4). Sequence analysis of cDNA, real-time PCR and Western blot analysis of hZnT4, carried out on control cells and cells from unrelated mothers of two infants with zinc deficiency, showed no differences. The hZnT4 gene was highly expressed in mouthwash buccal cells compared with lymphoblasts and fibroblasts. The hZnT4 protein did not co-localise with intracellular free zinc pools, suggesting that hZnT4 is not involved in transport of zinc into vesicles destined for secretion into milk. This observation, combined with phenotypic differences between the "lethal milk" mouse and the human disorder, suggests that the "lethal milk" mouse is not the corresponding model for the human zinc deficiency condition.

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“…Acrodermatitis enteropathica has been described in breast-fed infants related to low zinc levels in the mothers [9][10][11]. Moynahan [5] reported zinc deficiency in an infant suffering from AE and lactose intolerance.…”

Section: Discussionmentioning

confidence: 99%

Acrodermatitis enteropathica: Case report analyses of zinc metabolism electron microscopic examination and immune function

Gözdaşoĝlu

Taçyıldız

Günlemez

et al. 2000

J. Trace Elem. Exp. Med.

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Symptomatic zinc deficiency in breast‐fed term and premature infants

Cited by 69 publications

References 0 publications

Poor Zinc Status in Early Infancy among Both Low and Normal Birth Weight Infants and Their Mothers in Delhi

Poor Zinc Status in Early Infancy among Both Low and Normal Birth Weight Infants and Their Mothers in Delhi

Analysis of zinc transporter, hZnT4 ( Slc30A4 ), gene expression in a mammary gland disorder leading to reduced zinc secretion into milk

Acrodermatitis enteropathica: Case report analyses of zinc metabolism electron microscopic examination and immune function

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