Acquired acrodermatitis enteropathica in Child
It appears that zinc is required for the orderly proliferation of keratinocytes. Additionally, low tissue zinc is associated with the overproduction of inflammatory cytokines and reactive mediators.
The disease occurs in all age groups and there is no predilection by sex.
Decreased absorption of zinc is associated with inadequate dietary intake due to low caloric diets, anorexia nervosa, vegetarian diets, and diets high in phytates that bind zinc (typical of cereal grain-based diets common to parts of the Middle East and North Africa). Total parenteral nutrition (TPN) with inadequate zinc supplement is a known cause of deficiency. Malabsorption related to inflammatory bowel disease, celiac sprue, cystic fibrosis, and numerous bariatric procedures also leads to zinc deficiency. Chronic diarrhea, along with chronic liver and/or renal disease (nephrotic syndrome), are each risk factors for deficiency.
Medications associated with zinc deficiency include proton pump inhibitors (decrease absorption) and loop diuretics (increase loss). Some angiotensin converting enzyme (ACE) inhibitors and calcium channel blockers have also been implicated.
Identical clinical findings may result from hereditary acrodermatitis enteropathica, a rare autosomal recessive disease caused by abnormal zinc absorption due to a transport deficiency across the small intestine.
E60 – Dietary zinc deficiency
12602008 – Acquired acrodermatitis enteropathica
Differential Diagnosis & Pitfalls
- Linear IgA dermatosis
- Glucagonoma syndrome
- Necrolytic acral erythema – secondary to amino acid or essential fatty acid deficiency
- Seborrheic dermatitis
- Atopic dermatitis
- Acrokeratosis paraneoplastica (Bazex syndrome)
- Telogen effluvium (no club hairs) – acrodermatitis enteropathica has broken hairs