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Zinc-dependent chemotactic defect in an infant with acrodermatitis
Archives of Disease in Childhood
|December 1, 1980
Summary
A 5-month-old infant experienced acrodermatitis enteropathica after weaning. Zinc supplementation rapidly resolved symptoms and corrected immune defects, highlighting zinc's crucial role in infant immunity.
Area of Science:
- Pediatric Medicine
- Immunology
- Nutritional Science
Background:
- Acrodermatitis enteropathica (AE) is a rare genetic disorder of zinc absorption.
- Acquired zinc deficiency can occur due to inadequate dietary intake or absorption issues.
- Infant nutrition transitions, such as weaning, can impact nutrient status.
Observation:
- A 5-month-old infant presented with clinical signs of acrodermatitis enteropathica upon weaning from breast milk to cow's milk.
- The infant exhibited low plasma zinc concentrations.
- Immune function assessment revealed normal T- and B-lymphocyte activity but severely impaired neutrophil chemotaxis.
Findings:
- Oral zinc sulfate administration (40 mg daily) led to rapid clinical improvement of the skin lesions.
- Plasma zinc levels were restored to normal following zinc supplementation.
- Neutrophil chemotaxis function normalized completely after zinc treatment, indicating reversal of the immune defect.
Implications:
- This case underscores the importance of adequate zinc levels for proper immune function, particularly neutrophil chemotaxis, in infants.
- Zinc deficiency, even when acquired, can manifest with significant dermatological and immunological consequences.
- Dietary zinc monitoring and supplementation should be considered during infant weaning and in cases of suspected zinc deficiency.