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Concurrence of Acrodermatitis Enteropathica and Eczema Herpeticum in a Child with Atopic Dermatitis
Budi Satria1, WenChieh Chen2, Hardyanto Soebono1
1Department of Dermatology and Venereology, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada/Dr. Sardjito Hospital, Yogyakarta, Indonesia.
Insights
Acrodermatitis enteropathica (AcE), a zinc deficiency disorder, and eczema herpeticum can present similarly in children. Early diagnosis and treatment with oral zinc and acyclovir led to rapid symptom resolution in an 11-year-old boy.
Area of Science:
- Pediatric Dermatology
- Genetic Disorders
- Infectious Diseases
Background:
- Acrodermatitis enteropathica (AcE) is a rare genetic disorder of zinc malabsorption due to SLC39A4 mutations.
- Eczema herpeticum involves disseminated herpes simplex virus infection, often on atopic dermatitis (AD) skin.
- Distinguishing AcE from other eczematous conditions can be challenging.
Abstract:
Acrodermatitis enteropathica (AcE) is a rare, autosomal recessive inherited disorder caused by mutation of the SLC39A4 gene coding for zinc transport protein (ZIP 4). The disease appears during childhood especially in breastfeeding or post-breastfeeding infant. Eczema herpeticum refers to a disseminated skin infection of herpes simplex virus that usually leads to vesicular eruptions commonly seen on a background of atopic dermatitis (AD). We describe an 11-year-old boy with periorificial erosions in periorbital, perinasal, perioral, perineal, and gluteal areas, accompanied with itchy vesicles, some covered with hemorrhagic crusts. A clinical diagnosis of AcE and eczema herpeticum with AD was supported by typical lesions and acute and chronic eczematous changes found mainly in the flexural aspects of extremities, which is diagnostic of AD. Laboratory findings showed anti HSV1 IgG (23.43) and high levels of IgE (478.9 IU/L). There was no multinucleated giant cell in the Tzanck test. Skin histology was compatible with AcE. Direct immunofluorescent examination showed no deposits of IgG, IgM, IgA, or complement. Complete resolution occurred within 2 weeks of acyclovir and oral zinc supplementation.
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