Transient zinc deficiency in a breast fed, premature infant

A 5-month-old-male was observed for an acrodermatitis enteropathica-like skin eruption evolving since the second month. He was born prematurely at 27 weeks and his neonatal course was complicated by respiratory distress syndrome, sepsis and subependimary haemorrhage. He was fed with breast milk from the second day of life, fortified initially by a protein mineral supplement containing zinc. Serum zinc concentration was low and the mother's serum and milk had normal zinc values. Oral zinc supplementation was introduced with total clearing after three weeks. Treatment lasted 22 months and no relapse was observed after discontinuation. Premature infants have a negative zinc balance mainly secondary to inadequate stores and high requirements. The relevance of these factors is illustrated by the present case where symptomatic zinc deficiency developed despite maternal milk with normal zinc content and a milk fortifier containing zinc.     

Acrodermatitis enteropathica in full-term breast-fed infant

BACKGROUND: Acrodermatitis enteropathica is a rare autosomal recessive disorder, caused by impaired absorption of zinc from the gastrointestinal tract. Symptoms of acrodermatitis enteropathica occur within the first few months after birth and tend to appear shortly after discontinuation of breast-feeding. We report a breast-fed infant with acrodermatitis enteropathica. CASE REPORT: A full term, 4-month-old girl, consulted in dermatologic department for persistent and refractory anogenital lesions since the age of 1 month, with progressive erythematous, vesiculous and squamous lesions, sometimes erosive in a peri orificial and acral pattern. She was calm and healthy baby. She was breast feeding. The diagnosis of acrodermatitis enteropathica was confirmed by decreased plasma zinc level (14 microg/100 ml). Breast milk zinc levels was low (46 microg/100 ml), as plasma zinc level of the mother (94 microg/100 ml). A genetic study showed that she was homozygous for the mutation, whereas her brother and parents were heterozygous. She was given zinc sulphate, and her condition has improved significantly. DISCUSSION: Acrodermatitis enteropathica is characterized by a characteristic clinical feature and the diagnosis is confirmed by decreased plasma zinc level. Acrodermatitis enteropathica in exclusively breast fed infant is rare, it was essentially reported in premature babies. Our case report is particular because it's concerning a full-term breast-fed infant, with zinc deficiency in breast milk and mother's decreased plasma zinc level.     

Transient Neonatal Zinc Deficiency Caused by a Novel Mutation in the SLC30A2 Gene

This is a case report of a 4‐month‐old full‐term, fully breastfed boy who presented with a persistent periorificial and groin rash associated with poor weight gain and irritability. His serum zinc level was low. The mother's breast milk zinc level was found to be low despite her serum zinc levels being normal, confirming the diagnosis of transient neonatal zinc deficiency. Mutational analysis revealed a novel mutation in the mother's SLC30A2 gene, which encodes a zinc transporter expressed in mammary gland epithelial cells.     

Transient zinc deficiency syndrome in a breast-fed infant due to decreased zinc in breast milk (type II hypozincemia of infancy): A case report and review of the literature

Type II hypozincemia of infancy is a rare, hereditary zinc deficiency occurring in infants while exclusively on breast feeding. It is caused by defective transfer of zinc into breast milk. Only a few dozen cases have been reported. A 6-month-old, full-term, breast-fed female infant presented with a 3-week history of erythematous to dusky red papules and annular plaques over the perioral and diaper area as well as the digits. The eruption was accompanied by poor appetite and irritable crying. Serum zinc was low (4.896 μmol/L, normal = 10.71?18.36 μmol/L) in the patient but was normal in the mother. Interestingly, the zinc level in the breast milk was very low (2.142 μmol/L; normal postpartum zinc = 18.36 μmol/L at 6 months). Histopathology of a skin biopsy specimen showed spongiotic psoriasiform dermatitis with pallor of superficial keratinocytes, consistent with deficiency disease. With oral zinc sulfate supplement, her skin lesions improved significantly within 4 days. Type II hypozincemia needs to be differentiated from the classical hereditary acrodermatitis enteropathica, which typically develops symptoms after weaning because of poor intestinal absorption of zinc in the affected infants. Mutations in zinc transporter genes have been detected in SLC39A4 (Zip4) and SLC30A2 (ZnT2), respectively, in classical acrodermatitis enteropathica and type II hypozincemia. No mutation was found in these two genes in the present pedigree. Therefore, the genetic defect in our patient might involve other zinc transporter genes.     

Transient symptomatic zinc deficiency in a breast-fed preterm infant

Abstract:  Transient, symptomatic zinc deficiency in breast-fed, low-birthweight infants is a rare, but probably underrecognized disorder hallmarked by periorificial and acral dermatitis. Unlike in acrodermatitis enteropathica, symptoms disappear when nursing ends. We report a breast-fed, preterm infant with demarcated, erythematous, and exudative patches with overlying crusts on the perioral, perianal, and acral areas. Laboratory investigations revealed lowered zinc levels in the infant's serum, but normal levels in his mother's milk. Oral zinc supplementation resulted in total clearing of skin lesions within 4 weeks. Our patient's presentation illustrates the importance of zinc in rapidly growing preterm infants and aims to stimulate awareness for this disorder. Symptomatic zinc deficiency can be easily diagnosed by careful examination and effectively treated with oral zinc substitution.     

Transient Zinc Deficiency in a Full-Term Breast-Fed Infant of Normal Birth Weight

A full-term male infant was seen at age 5 months with symptomatic zinc deficiency. He was breast fed and the mother's milk zinc levels were low. The infant responded to oral zinc supplements and has continued to be asymptomatic for 12 months after their withdrawal. This is the first report of transient zinc deficiency in an otherwise healthy, breast-fed, full-term infant of normal birth weight.     

Unique presentation of transient zinc deficiency from low maternal breast milk zinc levels

We report full‐term siblings with a unique clinical presentation of polycyclic papulosquamous plaques secondary to transient zinc deficiency due to low maternal breast milk zinc levels. We present this case to highlight this unique presentation of zinc deficiency in breastfed infants.     

Symptomatic zinc deficiency in breast-fed premature infants

We report two breast-fed premature infants who developed transient symptomatic zinc deficiency with scaly erythema of cheeks and napkin area, 9-13 weeks after birth. Serum zinc concentrations were 3.6 and 4.8 mumols/l, and the lesions healed rapidly in response to oral zinc supplements. Both mothers had low breast-milk zinc levels (2.3 and 3.2 mumols/l at 21 and 15 weeks respectively). The infants were both initially misdiagnosed as having eczema and infection. Premature infants are in negative zinc balance and though the additional factor of a low maternal breast milk zinc concentration may be necessary to provoke symptoms, rashes developing in such infants in the months following premature birth should raise the suspicion of zinc deficiency.     

Symptomatic zinc deficiency in a breast-fed, premature infant

Hypozincemia and clinical features of acrodermatitis enteropathica developed in a breast-fed, premature infant at 6 months of age. Maternal breast milk zinc levels were normal at birth and at the time of appearance of zinc deficiency in the infant. Zinc supplementation administered orally resulted in rapid improvement. Seven premature infants with hypozincemia and transient symptomatic zinc deficiency have been previously described. In contrast with this case, the other infants received feedings with low zinc content.     

A Diagnostic Challenge: A Case of Acrodermatitis Enteropathica without Hypozincemia and with Maternal Milk of Low Zinc Level

Abstract: Acrodermatitis enteropathica is a rare and distinct form of zinc deficiency with a requirement of life‐long zinc supplementation and inherited in a recessive manner. Transient nutritional zinc deficiency is also a well known condition mimicking acrodermatitis enteropathica like skin changes in preterm and term infants who are generally breastfed with a low level of zinc containing milk. Here, a 4‐month‐old male, term and fully breastfed acrodermatitis enteropathica case without hypozincemia and with maternal milk of low zinc level is presented.     

AN ACQUIRED FORM OF ACRODERMATITIS ENTEROPATHICA DUE TO LONGTERM LACTOSE-FREE MILK ALIMENTATION

A 4-month-old boy, fed on lactose-free milk for the treatment of intractable diarrhea for about 3 months, developed acrodermatitis enteropathica-like skin lesions. All the symptoms dramatically disappeared 2 weeks after switching from this milk to a general cow's milk formula, and his low serum zinc level also rapidly returned to normal. The zinc deficiency seen in this case was presumed to be closely related to longterm lactose-free milk alimentation. Acrodermatitis enteropathica, a human zinc deficiency, should be classified into two types, hereditary and acquired. The latter form can develop from intravenous hyperalimentation, longterm lactose-free milk alimentation and longterm penicillamine administration.     

Acquired zinc deficiency in a breast-fed premature infant

Zinc deficiency that was diagnosed at 14 weeks of age developed in a breast-fed premature infant. There was a rapid response to zinc supplements (20 mg/day) and therapy was stopped after three weeks without recurrent disease. The maternal breast milk had a low level of zinc and this could not be corrected by oral zinc supplements.     

Uptake of Pyrene in a Breast-Fed Child of a Mother Treated with Coal Tar

Abstract:   A woman was treated for atopic dermatitis with coal tar containing ointments. Coal tar containing ointments contain genotoxic polycyclic aromatic hydrocarbons. Over a period of 50 days the accumulated dose of different coal tar containing ointments treatments corresponded to 993 mg of pyrene and 464 mg of benz[a]pyrene. During this treatment she gave breast milk to her 3-month-old daughter. Analysis of urine samples from the breast-fed child showed elevated levels of urinary excretion of a metabolite of pyrene (1-hydroxypyrene, 1-OHP). These levels were in the same range as urinary excretion levels of this metabolite observed in the mother's urine. As no pyrene was observed in breast milk at a limit of determination of 0.0035 μmol/L, transfer of pyrene from mother to child via breast milk is not likely. Also, a low level of 1-hydroxypyrene observed in the mother's milk did not account for the observed urinary excretion levels in the child. It must therefore be assumed that pyrene was transferred from mother to child via another route, presumably direct skin-to-skin or skin-to-mouth contact. Dermatologists should inform their patients who receive treatment with coal tar containing ointments of the risk of transfer of polycyclic aromatic hydrocarbons by skin-to-skin or skin-to-mouth contact.     

Transient Zinc Deficiency in Two Full-term Breast-fed Siblings Associated with Low Maternal Breast Milk Zinc Concentration

Symptomatic zinc deficiency developed in an exclusively breast-fed, full-term infant. Her older brother had also developed zinc deficiency while being exclusively breast-fed. Breast milk zinc concentrations were low throughout lactation, and this inadequacy is the likely cause of the deficiency in both infants.     

Acquired zinc deficiency in full-term newborns from decreased zinc content in breast milk

Zinc deficiency occurs in children when the demand for zinc exceeds its supply. Malnutrition, prematurity, total parenteral nutrition dependence, and burns increase the demand for zinc, whereas congenital malabsorption syndromes represent clinical situations where less zinc is supplied to the growing child. Clinical recognition of acral eczematous lesions, alopecia, and gastrointestinal tract symptoms in settings of the aforementioned medical history often lead to the diagnosis. Zinc deficiency in healthy, full-term, breast-fed infants can occur. The cause of these deficiencies has been attributed to decreased zinc levels in maternal breast milk. We present a case of acquired zinc deficiency in a healthy breast-fed infant, with a review of the English language literature of reported cases.     

Food allergy in atopic eczema I. The effect of maternal diet on breast-fed babies with eczema

Eczema in infants solely breast fed may be caused by food proteins transmitted through mother's milk (Warner, 1980). By radioimmunoassay we identified traces of cow's milk and egg proteins in human milk 2–4 h after oral challenge. Sixty-nine exclusively breast-fed infants with eczema and 36 controls were then studied. The infants' rashes were classified as 'definite atopic eczema' (DAE), 'possible atopic eczema' (PAE) and 'atopic eczema unlikely' (AEU). All were skin prick-tested against 12 common antigens including six foods. Thirty-five mothers who were breast feeding eczematous infants then completed controlled trials of cows' milk and egg exclusion diets.
Sixty-nine per cent of infants with DAE, 37% with PAE, 25% with AEU and 8% of controls gave positive skin tests to food antigens, in all but three cases to egg and cows' milk. Thirty of 35 (86%) infants did not benefit from a maternal cow's milk and egg exclusion diet. In five, however, exclusion appeared to be effective and double-blind challenge provoked eczema in all five and diarrhoea and colitis in one.
Although half of exclusively breast-fed infants with eczema (DAE and PAE) show cutaneous hypersensitivity to cows' milk or egg protein, only a minority improve if mothers avoid these foods.     

A novel homozygous mutation p.E88K in maternal SLC30A2 gene as a cause of transient neonatal zinc deficiency

The SLC30A2 gene encodes zinc transporter ZnT2, which is indispensable for the transport of zinc into the breast milk in the mammary gland. Transient neonatal zinc deficiency (TNZD) is caused by a mutation in the maternal SLC30A2 gene and has a clinical presentation similar to that of acrodermatitis enteropathica (AE). We described the case of a Chinese infant who presented with AE-like lesions 10 days after birth. Sanger sequencing of the AE-causing gene SLC39A4 revealed no mutations in genomic DNA from the infant, excluding the possibility of AE. Detection of the mother's breast milk showed a significantly lower zinc level. Thus, SLC30A2 sequencing was performed on her genomic DNA and a previously unreported homozygous c.262G > A (p.E88K) mutation was disclosed. Functional analysis suggested the novel mutation could lead to a strong disruption of zinc secretion, which indicated a complete loss of function in the ZnT2 protein. We finally diagnosed the infant with TNZD. To the best of our knowledge, this is the first case of TNZD caused by a homozygous mutation in the maternal SLC30A2 gene. Compared to the heterozygous condition, a homozygous mutation seems to result in a more significant decrease in zinc secretion and a more rapid onset of TNZD.     

Transient Neonatal Zinc Deficiency Due to a New Autosomal Dominant Mutation in Gene SLC30A2 (ZnT‐2)

Transient neonatal zinc deficiency (TNZD) has a clinical presentation similar to that of acrodermatitis enteropathica but is caused by a low zinc concentration in maternal breast milk. TNZD becomes clinically evident during breastfeeding and is resolved by weaning and the introduction of complementary nutrition. We present a 4‐month‐old girl with TNZD due to a new autosomal dominant mutation (663delC) in the maternal SLC30A2 gene not previously described in the literature.     

Acrodermatitis enteropathica: a novel SLC39A4 gene mutation found in a patient with an early-onset

We report the case of a 3-month-old full-term, breast-fed infant with clinical and laboratorial findings consistent with acrodermatitis enteropathica. In addition, the mother had low zinc levels in her breast milk. Mutation analysis revealed a novel insertion in the SLC39A4 gene.     

Zinc and skin: a brief summary

Zinc is an essential trace element that is an integral component of many metallo-enzymes in the body and thus serves many biological functions. The clinical presentation of zinc deficiency varies and depends on serum zinc level. Whereas a significantly low serum zinc level results in clinical features similar to acrodermatitis enteropathica, mild hypozincemia presents with a less characteristic appearance; hence it may be underdiagnosed. Recognition of various cutaneous lesions is required for suspecting and identifying cases of zinc deficiency. Although many laboratory tests are useful, therapeutic response in suspected cases remains the gold standard of diagnosis. Serum zinc estimation alone is not very reliable because disease activity may not necessarily correlate with serum zinc level. Zinc supplementation results in a rapid response and the skin lesions heal without permanent sequelae. However, pigmentary alterations may persist longer. Predisposing factors should be identified and corrected. This brief review summarizes the identification and management of clinical zinc deficiency.