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.     

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.     

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.     

Acne treatment with oral zinc and vitamin A: effects on the serum levels of zinc and retinol binding protein (RBP).

The serum levels of zinc, vitamin A and retinol binding protein (RBP) were studied in 75 acne patients before and during oral treatment with zinc, vitamin A or placebo. In the zinc-treated patients an increase in the mean serum zinc level was seen after 2 weeks, when also the first clinical improvement occurred. After 4 weeks the zinc level had increased by about 30% and no further significant increase was observed during 3 months of treatment. In 33 healthy subjects there was an increase of 14% after 4 weeks of zinc therapy. Vitamin A and placebo induced no significant changes in the serum zinc status. Prior to therapy the serum levels of vitamin A and RBP were lower in the acne patients than in the controls. Zinc + vitamin A treatment raised the serum RBP value to normal after 4 weeks. In patients given vitamin A alone, a probable increase in RBP was achieved. Zinc and placebo treatment did not change the serum level of RBP.     

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 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.     

Acrodermatitis enteropathica in a full-term breast-fed infant: case report and literature review

A male full‐term infant, who had been exclusively breast‐fed since birth, at 2 months of age developed an erythematous, scaling eruption involving the face (in a periorificial distribution, i.e. mouth, nose, ears, and eyes), hands, and feet, which did not respond to treatment with topical corticosteroids and oral antimicrobials. He was first seen at our institution at 5 months of age ( Figs 1 and 2 ). He had been irritable for the last 2 weeks, but had no diarrhea, alopecia, or anogenital lesions. A clinical diagnosis of acrodermatitis enteropathica was confirmed with a serum zinc level of 41.2 µg/dL (normal, 70–120 µg/dL). His mother had low–normal serum (70.5 µg/dL; normal, 70–120 µg/dL) and normal milk (0.43 µg/mL; normal, 0.2–0.72 µg/mL) zinc concentrations. Within 7 days of starting therapy with zinc sulfate, 10 mg/kg/day, all cutaneous lesions had resolved ( Fig. 3 ).

Figure 1 Open in figure viewer PowerPoint Infant at 5 months of age showing an erythematous, scaling eruption involving the face (periorificial distribution, i.e. mouth, nose, and eyes) and hands     

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.     

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.     

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.     

Restrictive dermopathy in a Turkish newborn

A 4-day-old boy presented with tight, translucent skin, prominent vessels, skin erosions, and dysmorphic findings, including hypertelorism, antimongoloid axis, sparse eyelashes and eyebrows, pinched nose, natal teeth, microretrognathia, and an "o-shaped" mouth. Multiple joint contractures, dysplastic clavicles, and thin ribs were also observed. He died at 2 weeks of age of respiratory distress. The patient was diagnosed as being affected with restrictive dermopathy, which is a rare, lethal genodermatosis caused by recessive mutations of the zinc metalloproteinase ZMPSTE24 gene or less frequently, by dominant lamin A/C gene mutations. Direct sequencing of the ZMPSTE24 gene was performed, and the most common, homozygous, inactivating mutation in exon 9 was identified in the patient (c.1085_1086insT; p.Leu362PhefsX19). Autosomal recessive transmission was confirmed by parental DNA analysis. After genetic counseling, a prenatal diagnosis could be performed during the subsequent pregnancy. ZMPSTE24 screening was performed by direct sequencing and fluorescent fragment analysis on DNA derived from a chorionic villus sample after exclusion of maternal contamination. The fetus had inherited both normal parental alleles, avoiding the recurrence of the disease.     

Ultrastructural changes of zinc deficient rat epidermis: an electron microscopic study

Zinc deficiency was produced in rats by feeding them a diet containing 0.5 mg zinc per kg. After 2 weeks the zinc-deficient rats showed markedly stunted growth as compared with control rats receiving an identical diet supplemented with 50 mg zinc per kg. After about 3 weeks all rats in the zinc-deficient group developed a greasy, coarse and scaly coat with dispersed, denuded, eczematous patches. After 32 days the animals were sacrificed and skin specimens were obtained from the abdominal area. Electron microscopy showed two different patterns of epidermal changes: (A) edematous cell bodies and cell organelles, degenerate nuclei, while desmosomes were well preserved: (B) parakeratotic and dyskeratotic cells with sparse keratohyalin granules, abnormal keratinosomes, poorly developed desmosomes, and disintegrated mitochondria in the upper part of the epidermis. In the lower part, keratinocytes contained numerous ribosomes and thick chromatin aggregates in the nuclei. Dendritic cells were disintegrated in pattern A, while they appeared normal in pattern B. In both patterns mitochondria showed vacuoles and a lack of DNA granules. A transient form of type A and B changes was also observed.     

Netherton's syndrome in siblings

We report the perinatal presentation and evolution of Netherton's syndrome in siblings. The first patient, a female infant, presented with asphyxia at birth due to aspiration of desquamated scale, non-bullous ichthyosiform erythroderma, and hypernatraemic dehydration which she had for several days. Subsequently, she failed to thrive, with recurrent bacterial infections until 5 months of age, and very high serum IgE levels (1200 U/mL). Trichorrhexis invaginata and pili torti were identified at 18 months. The second patient was the younger brother of the first. Hydramnios and hyperechoic material in the amniotic fluid were observed by ultrasound at 35 weeks gestation, and he was delivered by elective Caesarian section at 40 weeks. At birth, no hair abnormality was demonstrated but, like his sister, his body was covered with thick caseous material, and he was erythrodermic. He failed to thrive, but serum IgE levels were normal until 5 months of age. Typical trichorrhexis invaginata was not observed until 7 months of age. Thus, the hair abnormality and high serum IgE levels in Netherton's syndrome appear late relative to the ichthyosiform erythroderma.     

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.     

Oral 13, An unexplained disorder of keratinization

A 6-year-old boy initially presented at the age of 1 week with perineal and perianal rash. The rash was persistent and at the age of 8 months he developed gastroenteritis. He was found to have borderline zinc deficiency. However, there was no improvement with zinc supplementation and the rash progressed to well-demarcated psoriasiform plaques involving the perianal area, penis, scrotum, upper thighs, face, axillae, right elbow and neck. He also developed palmoplantar keratoderma. Initially the hair was sparse and brittle. He developed recurrent chest and skin infections. There was a family history of malignant hyperpyrexia and mitochondrial myopathy.
Skin biopsy was nonspecific, showing chronic superficial dermatitis. Analysis of skin and blood for recognized keratin and connexin disorders did not show any abnormalities. Gastroenterology investigations revealed oesophagitis, gastritis and patchy pancolitis. Routine blood tests were normal. Lactate levels, acylcarnitine profile, organic acids, tubulopathy screen, glycosaminoglycans, biotinidase, betamethylcarboxyl CoA carboxylase, holocarboxylase synthetase, prolidase and tyrosine aminotransferase levels were normal. Autoimmune screen and immunological investigations were normal. Blood tests for coeliac disease were negative. Electromyography and DNA analysis for mitochondrial myopathy were normal. Sweat studies and cystic fibrosis gene analysis were normal. DNA analysis for malignant hyperpyrexia was negative.
His skin condition gradually improved on treatment with acitretin 10 mg three times a week and topical emollients. He is still troubled by recurrent infections. His gastroenteritis is well controlled by an oligoantigenic diet.
We are grateful to Professor John Harper and Professor David Kelsall for their help in managing this child.     

A dermatitis-eosinophilia syndrome. Treatment with methylprednisolone pulse therapy

A 47-year-old man had a generalized, eczematous erythroderma and eosinophilia one week after a wasp sting. These changes persisted for four months despite intensive topical therapy and oral corticosteroids. He was then given corticosteroid pulse therapy with methylprednisolone sodium succinate (2 g, intravenously). One week later, a second pulse treatment was administered. This therapy was followed by permanent resolution of the dermatitis within two weeks.     

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.     

Clinical efficacies of topical agents for the treatment of seborrheic dermatitis of the scalp: A comparative study

Previous studies have shown that topical steroid and shampoo containing zinc pyrithione provide clinical benefits for treatment of scalp seborrheic dermatitis. But the clinical efficacy of topical tacrolimus, a newly developed calcineurin inhibitor on seborrheic dermatitis, is not well investigated yet. We wanted to compare the clinical efficacy of topical tacrolimus with that of conventional treatment (zinc pyrithione shampoo and topical betamethasone) for treatment of seborrheic dermatitis of the scalp. Patients with seborrheic dermatitis of the scalp were randomly allocated to receive topical betamethasone, topical tacrolimus or zinc pyrithione shampoo. Some patients were instructed to continue the treatments for 8 weeks and the others to discontinue the treatments at week 4. We evaluated the efficacy using a clinical severity score, dandruff score and sebum secretion at baseline, week 4 and week 8. All treatment groups showed significant improvements in clinical assessment after 4 weeks. While the patients treated by zinc pyrithione improved continuously even after cessation of the treatment, the patients treated by betamethasone lotion or tacrolimus ointment were aggravated clinically. Topical tacrolimus was as effective as topical betamethasone, and showed more prolonged remission than topical betamethasone. To treat seborrheic dermatitis of the scalp, we think that the combination therapy of topical steroid or topical tacrolimus, and zinc pyrithione is recommended.     

A randomized,double‐blind,placebo‐controlled trial to determine the efficacy and safety of lactoferrin with vitamin E and zinc as an oral therapy for mild to moderate acne vulgaris

Lactoferrin is an iron‐binding milk‐derived protein that has shown antibacterial and anti‐inflammatory effects in vitro and in vivo. The objective of this study was to determine the efficacy and safety of lactoferrin, combined with vitamin E and zinc, for mild to moderate acne vulgaris. In this randomized, double‐blind, placebo‐controlled trial, 168 subjects aged 13–40 years old were randomly assigned to take either a capsule formulation containing lactoferrin with vitamin E and zinc or placebo twice a day for 3 months. The primary outcome measure was a reduction in the number of acne lesions compared to placebo. A total of 164 subjects completed the study per protocol. The lactoferrin group (n = 82) showed a significant median percent reduction in total lesions as early as 2 weeks (14.5%, P = 0.0120), with the maximum reduction occurring at week 10 (28.5%, P < 0.0001) compared to placebo group (n = 82). Maximum reduction in comedones (32.5%, P < 0.0001) and inflammatory lesions (44%, P < 0.0001) was also seen at week 10 compared to placebo. Sebum scores were improved by week 12. No adverse events were observed during the trial. A twice daily regimen of lactoferrin with vitamin E and zinc significantly reduced acne lesions in people with mild to moderate acne vulgaris.