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.     

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.     

Transient zinc deficiency in a breast-fed premature infant

Symptomatic zinc deficiency developed in a breast-fed premature male infant of 31 weeks gestation. At 13 weeks of age he presented with diarrhoea, irritability and an eruption identical to acrodermatitis enteropathica. Breast milk zinc concentrations were low. His course was complicated by milk protein intolerance. After 7 weeks, zinc supplementation was ceased without recurrence of disease.     

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 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.     

Acquired dermatitis due to zinc deficiency in a premature infant

A case of dermatitis with lesions reminiscent of enteropathic acrodermatitis of the premature of low gestational age is presented. The condition responded dramatically to oral zinc sulphate therapy.     

Acquired zinc deficiency in two breast-fed mature infants

Zinc deficiency was diagnosed in a breast-fed mature infant and her sister. In both infants the characteristic dermatitis appeared on the face and buttocks around 10 weeks of age. It responded rapidly to zinc supplements. Their mother's serum zinc level was slightly low but her milk was found to be remarkably low in zinc. Oral zinc supplementation could correct only her serum zinc level but not her low breast milk zinc level. Therefore the mother's deficiency in the transfer process of zinc from serum to breast milk was suspected as a cause of the skin changes in her children. These cases indicate that even mature infants, who feed exclusively on mother's milk, run a risk to develop zinc deficiency, if the concentration of zinc in the breast milk is very low.     

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.     

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.     

Symptomatic zinc deficiency in a one-year-old child precipitated by changing from formula to cow's milk.

The case of a one-year-old girl with symptomatic zinc deficiency is presented. She had been misdiagnosed as having impetigo and/or candidiasis and had been treated with topical antifungal agents and both oral and topical antibiotic agents without success during the four months before she presented. Zinc replacement led to rapid improvement. Her nutritional history suggests that weaning from formula to cow's milk precipitated her eruption. The clinical findings, differential diagnosis, and treatment of zinc deficiency are reviewed.     

Tinea versicolor in a premature infant

Tinea versicolor (TV) is a fungal skin infection that classically affects adolescents and young adults. Occasionally, it may be seen on the face of infants. We report an unusual case of widespread cutaneous TV in a premature infant.     

Skin changes in alimentary zinc deficiency caused by artificial infant food

We report on 2 non-related newborn children who developed erythematosquamous skin eruptions on both their faces and the extensor sides of their fingers at the 4th and 10th week after birth, resp. Both children had been fed upon hypoallergenic formulas since birth. Serum investigations revealed decreased zinc levels: 0.4 and 0.17 mg/l, resp. (normal values: 0.59-0.96 mg/l). Following zinc substitution with zinc sulphate 10 mg daily for 3 days, the serum zinc levels of both children had increased to normal values and remained stationary during continued treatment with 3 mg zinc daily. The skin eruptions disappeared a few days after the start of treatment.