Acquired Zinc Deficiency Mimicking Acrodermatitis Enteropathica in a Breast-Fed Premature Infant

Abstract

We present a case of a transient acquired zinc deficiency in a breast-fed, 4-month-old-male prematurely born infant, with acrodermatitis enteropathica-like symptoms such as crusted, eroded, erythemato-squamous eruption in periorificial and acral patterns. The laboratory investigations showed low zinc levels in the infant’s and the mother’s serum and in the mother’s milk; genetic analysis did not show any mutation in the SLC39A4 gene, involved in acrodermatitis enteropathica. Acquired zinc deficiency is often found in premature infants because of their increased requirement, the low serum and milk zinc levels in breastfeeding women being also an important risk factor, as in this case. A prompt zinc supplementation is essential for the good prognosis of the disease.

Diet management in congenital diarrheas and enteropathies – general concepts and disease-specific approach, a narrative review

“…A mutation in SLC30A2 , a gene encoding the zinc transporter ZnT2, can lead to a decreased zinc secretion in breast milk and transient AE, such as in breastfed neonates [ 76 ]. Acquired forms of AE are variable and include zinc-deficient breast milk [ 77 ] or concurrent conditions such as malabsorptive disorders (e.g., cystic fibrosis, celiac disease, cholestatic liver disease) or in cases in which the duodenal surface area is bypassed (e.g. surgery, postpyloric/jejunal nutrition support) [ 73 , 74 ].…”

Acquired Zinc Deficiency in Preterm Infant Post-Surgery for Necrotizing Enterocolitis (NEC) on Prolonged Total Parenteral Nutrition (TPN)

“…Since Zn is required at all stages of a child’s development, severe Zn deficiency has been reported to lead to slower physical, cognitive, and sexual growth. It also manifests in skin disorders, immune compromise, and a higher frequency of acute illnesses in infants and children [ 1 , 7 , 8 ]. In the worst-case scenarios, Zn deficiency results in childhood stunting with an increased risk of morbidity as well as mortality in children [ 3 , 8 , 9 ].…”

“…Zn deficiency may be either inherited or acquired depending upon the point at which Zn metabolism is being affected [ 7 ] (See Figure 1 ). Inherited Zn deficiency usually arises as secondary to the genetic mutations in the zinc transporter genes.…”

“…Two of the important inherited Zn disorders have been characterized so far. One is due to mutation in the SLC39A4 gene, which codes for zinc transporter ZIP4 in the affected individual and leads to impairment in the absorption of zinc from the gastrointestinal tract and hence low serum levels of the Zn (<50 mcg/dL); this is referred to as acrodermatitis enteropathica (AE) [ 7 , 10 ]. The second is due to mutation in the mother’s SLC30A2 gene, which codes for the ZnT2 zinc transporter and leads to the reduced transport and secretion of zinc into breast milk; this disease is referred to as transient neonatal zinc deficiency (TNZD) [ 5 , 10 , 11 ].…”

“…Irrespective of the etiology of Zn deficiency, in its early stages all types exhibit the triad of clinical manifestations that include dermatitis, diarrhea, and alopecia [ 3 , 5 , 7 , 12 ]. Since, during fetal development, most of the Zn is acquired during the third trimester of the pregnancy, in preterm infants there is a high demand for Zn as a consequence of premature delivery [ 5 , 11 , 12 ].…”