4 Desferrioxamine-induced iron excretion in humans

doi:10.1016/S0950-3536(89)80020-4

Baillière's Clinical Haematology

Volume 2, Issue 2, April 1989, Pages 323-343

https://doi.org/10.1016/S0950-3536(89)80020-4 Get rights and content

Summary

Iron excretion in response to DF in humans is dependent upon the degree of iron overload, particularly of parenchymal liver cells. However, a number of variables, including ascorbate status, erythroid activity and liver disease, affect both the amount of iron mobilized and the route by which it is excreted. Faecal iron, derived from the bile, appears to arise from intracellular chelation of a transit iron pool related to hepatocyte iron stores, whereas urine iron may be derived from iron capable of exchanging with plasma transferrin at cell membranes of both hepatocytes and macrophages. Faecal iron predominates as iron stores return towards normal on regular chelation therapy. An understanding of the variables which influence iron excretion allows rational planning of long-term therapy with DF in patients with iron-loading anaemias. In young children a dose of 40–50 mg/kg given on five or six nights a week from the age of about 3 years is appropriate for prevention of serious iron loading. In older children the dose must be carefully tailored (by means of an individual urinary iron excretion dose-response curve) to achieve maximum safe chelation of pre-existing iron stores. In patients with slower rates of iron loading from excessive gastrointestinal iron absorption, intermittent use of DF infusions may be sufficient to maintain normal iron stores.

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