Acrodermatitis enteropathica

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Abstract
The 1st publication identifying acrodermatitis enteropathica [AE] as a definite disease (Danbolt and Closs, 1942) is reviewed. Later studies are briefly surveyed, resulting in the recognition of the disease as a Zn deficiency which can be effectively corrected by administration of small oral doses of Zn. This disease resembled Hallopeau''s disease and the clinical picture was incompatible with those of epidermolysis bullosa or monileasis; both these diagnoses had been applied to similar syndromes in the past. The disease characteristics are described. The disease may be caused by a primary affection of the intestinal tract (alkalosis intestini), which brings about changes of the metabolism, which are responsible for the different symptoms. The true nature of this disturbance remains unknown. The highly characteristic clinical picture described did not correspond to any of the designations previously used. Quinoline was successfully used to treat the symptoms, but it later became evident that long-term treatment with quinoline preparations could lead to retinopathy (with optic atrophy) in a few patients. Moynahan (1974) showed that administration of Zn to 8 patients with AE had had an excellent therapeutic effect. Probably, Zn medication must be continued indefinitiely. Disease due to Zn deficiency has long been known in veterinary medicine (Moynhan, 1974; Reich, 1976). In may domestic animals Zn deficiency may not only retard growth but also lower the the animal''s resistance to infection. Zn deficiency in domestic animals in general may give rise to symptoms very similar to those characteristic of AE. The history of the identification of the clinical picture of AE demonstrated that the disease was due to Zn deficiency, which could be effectively treated by oral administration of small quantities of Zn.

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