Zinc and di-iodohydroxyquinoline therapy in acrodermatitis enteropathica.

Abstract

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-

Physiology of Zinc: General Aspects

“…In our studies of one patient during commencement of zinc therapy, balance studies revealed that she retained approximately 120 mg of zinc in total which was less than 10% of her expected total body zinc (Jackson 1977). Thus it may be that the depletion of only a small specific "pool" of zinc (such as the membrane-bound zinc, as proposed by Bettger and O'Dell 1981, or the "exchangeable pool" of zinc described by Jackson et al 1984) is sufficient to produce severe zinc deficiency symptoms (see also Chap.…”

Acrodermatitis enteropathica

“…Since a considerable amount of zinc is secreted by the intestinal mucosa and pancreas it is also intriguing that there was no evidence of any increased loss of endogenous zinc in these patients. Metabolic balance studies of patients have shown net intestinal secretion of zinc in the untreated state which can be reversed by DIH or by large supplements of zinc orally (Aggett et al, 1978;Aggett et al, 1979) or by both (Jackson, 1977) to net absorption of the element. Hambidge and colleagues (1978) found a reduced concentration of zinc in a small intestinal biopsy from an untreated patient and postulated that, in Acrodermatitis enteropathica, intestinal uptake of zinc may be abnormal.…”

Clioquinol Synergistically Augments Rescue by Zinc Supplementation in a Mouse Model of Acrodermatitis Enteropathica

“…The preponderance of evidence suggests that this unique syndrome was not caused by CQ alone but was related to zinc deficiency and malnutrition [30], [34]. Later in the 70′s AE was recognized as a zinc deficiency disease [27] and it was understood that CQ was functioning as an ionophore for zinc [35], [36]. Thereafter, most AE patients were treated effectively with lifelong zinc supplementation but not with CQ.…”