SUMMARY A 25-year-old patient with acrodermatitis enteropathica who had been treated with di-iodohydroxyquinoline for 20 years was changed to zinc sulphate therapy and studied under full metabolic balance control for zinc, calcium, magnesium, and inorganic phosphorus. The results obtained indicate that there is only a small overall deficit of body zinc stores in this disease and that the function of di-iodohydroxyquinoline is to increase the amount of zinc absorbed and retained by the body.It has been shown that acrodermatitis enteropathica is an inherited zinc deficiency disorder (Barnes and Moynahan, 1973;Moynahan, 1975;Neldner and Hambidge, 1975)] but, the mechanism by which this deficiency occurs has not been satisfactorily ascertained. Lombeck et al. (1975), in acute loading tests, showed that the defect was a reduced absorption of zinc by the gut and not an increased excretion of zinc into faeces, urine or sweat. It was postulated by Moynahan (1974) that an oligopeptide chelated the ingested zinc to yield an insoluble complex, thus reducing the zinc available for absorption. Recently, Delves et al. (1975) have suggested that di-iodohydroxyquinoline acts by complexing the zinc ions and this complex is absorbed from the gut. External zinc balances before and after change of treatment do not appear to have been described. The aim of this work was to obtain information on the mechanism of the therapeutic effect of di-iodohydroxyquinoline in this disease and to obtain a measure of the deficiency of zinc in this patient.
PatientOur patient was a woman who had been diagnosed by Hare and Schlesinger (1955), at which time she had been started on di-iodohydroxyquinoline therapy, a gluten-free diet, and pancreatin. She was kept on regular follow-up, and six months later the gluten-