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Journal ArticleDOI

Deferoxamine (desferrioxamine). New toxicities for an old drug.

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TLDR
Iron is an esssential element for body homoeostasis, but there is no effective mechanism for elimination of an excess of this mineral, so deferoxamine (desferrioxamine) is currently the treatment of choice for iron overload states from both acute iron intoxication and transfusion-dependent anaemias.
Abstract
Iron is an essential element for body homoeostasis, but there is no effective mechanism for elimination of an excess of this mineral. Deferoxamine (desferrioxamine) is currently the treatment of choice for iron overload states from both acute iron intoxication and transfusion-dependent anaemias. The pharmacokinetics of deferoxamine are confounded both by its ability to chelate endogenous and exogenous iron and by the laboratory techniques used for its determination. Its iron-complex (ferrioxamine) has different pharmacokinetic properties. Because of its effectiveness, the use of deferoxamine is becoming more common, involving long term and high dose regimens. As a result of this, more and more toxicities that were not known in the past have been described and characterised. The most serious of these include hypotension, renal insufficiency, neurotoxicity, growth retardation and opportunistic infections: some of these side effects may be attributed to or aggravated by ferrioxamine. The pharmacological and toxicological literature on deferoxamine, and possible mechanisms for its toxicity, are reviewed and discussed.

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References
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Journal ArticleDOI

The biochemistry of desferrioxamine and its relation to iron metabolism.

TL;DR: The stability constants for various desferrioxamine-metal complexes compared with the constants for other chelating agents are listed in TABLE l.596 The higher the constant, the more stable the complex.
Journal ArticleDOI

Visual and Auditory Neurotoxicity in Patients Receiving Subcutaneous Deferoxamine Infusions

TL;DR: Of 89 patients receiving nightly subcutaneous deferoxamine for transfusion-dependent thalassemia major or Diamond-Blackfan anemia, 13 presented with visual loss or deafness of acute onset or both, and detailed ophthalmologic, audiologic, and evoked-potential studies uncovered abnormalities caused by neurotoxicity in 27 more.
Journal ArticleDOI

Deferoxamine: a reversible S-phase inhibitor of human lymphocyte proliferation

TL;DR: The binding of iron by deferoxamine likely causes an inhibition of ribonucleotide reductase activity, thereby preventing cells from completing the S phase of the cell proliferation cycle, and may have important experimental and therapeutic applications.
Journal ArticleDOI

Ocular toxicity of high-dose intravenous desferrioxamine

TL;DR: Desferrioxamine was given intravenously, at higher doses than previously reported, to counter the effects of transfusion-induced iron overload in four patients with beta thalassaemia major, and retinal abnormalities developed, presenting with night blindness and field defects.
Journal ArticleDOI

Effect of iron deficiency and desferrioxamine on DNA synthesis in human cells.

TL;DR: Phytohaemagglutinin‐stimulated lymphocytes from patients with chronic iron deficiency showed lower levels of all four deoxyribonucleoside triphosphates than normal lymphocytes, suggested that this may be due to reduced ribonucleotide reductase activity of the iron‐deficient cells.
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