Deferoxamine is isolated from Streptomyces pilosus. It binds iron avidly (Figure 57–3) but binds essential trace metals poorly. Furthermore, though competing for loosely bound iron in iron-carrying proteins (hemosiderin and ferritin), it fails to compete for biologically chelated iron, as in microsomal and mitochondrial cytochromes and hemoproteins. Consequently, it is the parenteral chelator of choice for iron poisoning. Deferoxamine plus hemodialysis may also be useful in the treat-ment of aluminum toxicity in renal failure. Deferoxamine is poorly absorbed when administered orally and may increase iron absorption when given by this route. It should therefore be admin-istered intramuscularly or, preferably, intravenously. It is believed to be metabolized, but the pathways are unknown. The iron-chelator complex is excreted in the urine, often turning the urine an orange-red color.
Rapid intravenous administration may result in hypotension. Adverse idiosyncratic responses such as flushing, abdominal discomfort, and rash have also been observed. Pulmonary compli-cations (eg, acute respiratory distress syndrome) have been reported in some patients undergoing deferoxamine infusions last-ing longer than 24 hours, and neurotoxicity and increased suscep-tibility to certain infections (eg, with Yersinia enterocolitica) have been described after long-term therapy of iron overload conditions (eg, thalassemia major).