Clinical Reference / Therapeutic Strategies / Acrodermatitis Enteropathica

Acrodermatitis Enteropathica

Zinc Deficiency

Zinc deficiency may be seen in infants (hereditary or acquired) or adults (acquired). Some breastfed infants, especially if born prematurely, may develop acrodermatitis enteropathica due to zinc deficiency in mother’s breast milk. These children improve when given standard formula with zinc, and may not require supplementation with zinc. Acquired zinc deficiency is seen in the postoperative period, in pregnancy, in patients with impaired zinc consumption, and in alcoholism. Zinc deficiency may result in typical dermatitis as well as nonhealing ulcers and recalcitrant infections. Secondary oral candidiasis (thrush) often complicates AE, and they may need to be treated simultaneously. Because zinc deficiency causes acrodermatitis enteropathica (AE), the therapeutic strategy is to replace zinc.


First Steps

  1. Prescribe oral zinc sulfate 220 mg two or three times a day with meals or fruit juice for children. In adults, 220 mg once or twice daily is usually adequate. (Children with hereditary AE have poor absorption and require higher oral doses than adults with acquired AE). Response begins to occur within days.
  2. Prescribe oral nystatin suspension or troches for Candida superinfections and to patients whose oral lesions are responding slowly to zinc supplementation alone.

Alternative Steps

Some cases of AE do not clear completely with oral zinc sulfate. Order a zinc level to confirm defective absorption. Parenteral supplementation at doses of 0.2 to 0.3 mg/kg zinc per day can be given.


Hyperzincemia, with zinc toxicity, can result from acute or prolonged overdosing with zinc. Dosages should be adjusted based upon regular (1-2 week) assessment of fasting plasma zinc levels (i.e., before the next oral dose).