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Deferoxamine

Deferoxamine, otherwise known as desferrioxamine or desferal, is a chelating agent used to remove excess iron from the body. It acts by binding free iron in the bloodstream and enhancing its elimination in the urine. By removing excess iron, the agent reduces the damage done to various organs and tissues, such as the liver. more...

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Deferoxamine is used to treat acute iron poisoning, especially in small children. Treatment with this agent is also frequently necessary in patients with certain types of chronic anemia (e.g. thalassemia and myelodysplastic syndrome) who require many blood transfusions, which can greatly increase the amount of iron in the body. Administration for chronic conditions is generally accomplished by subcutaneous injection (SQ) over a period of 8-12 hours daily. Administation of deferoxamine after acute intoxication may color the urine a pinkish red, a phenomenon termed "'vin rose urine".

Apart from in iron toxicity, deferoxamine is also used to treat aluminum toxicity (an excess of aluminum in the body) in certain patients.

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INTERFERON-[Gamma] PRIMES HUMAN ALVEOLAR MACROPHAGES FOR INCREASED INTERLEUKIN-1[Beta] RELEASE BY DECREASING BIOAVAILABLE IRON
From CHEST, 10/1/99 by Steven R Hays

Purpose: It has been demonstrated that decreasing intracellular iron levels by chelation with deferoxamine (DFA), increases the release of IL-1[Beta] from LPS-stimulated human alveolar macrophages (AM). IFN-[Gamma] has also been show to augment the LPS-stimulated release of IL-1[Beta] from LPS-stimulated human AM. We hypothesized that IFN-[Gamma] augments the release of IL-1[Beta] through a mechanism similar to that of DFA, that is, by reducing bioavailable intracellular iron. The purpose of this study was to demonstrate the effects of IFN-[Gamma] on intracellular bioavailable iron levels and the subsequent release of IL-1[Beta] by LPS-stimulated human AM.

Methods: Human AMs were recovered from subjects by bronchoalveolar lavage. Following pretreatment with 25U and 250U of IFN-[Gamma] for 1.0 h, the cells were exposed to LPS (0.01-1.0 ug/ml). Cells were harvested at 1.5, 5 and 20 hours. A sensitive redox-cycling, fluorometric assay was used to measure intracellular bioavailable iron. The release of IL-1[Beta] was measured by ELISA.

Results: IFN-[Gamma] pretreated cells demonstrated a dosedependent decrease (27 [+ or -] 6 % and 41 [+ or -] 9%) in intracellular bioavailable iron at 1.5 hours. There was a 38% augmentation of IL-1[Beta] release at 20 hours in IFNg pretreated cells.

Conclusion: IFN-[Gamma] reduces the bioavailability of iron in human AM within 90 minutes. These findings suggest that the ability of IFN-[Gamma] to prime macrophages for augmented IL-1b release is linked to its ability to lower the bioavailability of intracellular iron as we have shown previously with iron chelation.

Clinical Implications: This phenomena may have particular importance in the modulation of inflammation in lung diseases where macrophages acquire excess iron, such as those associated with smoking. Supported by: NIII IDcA P20 and KTEC

Steven R Hays, MD(*); B M Blumer and A R O'Brien-Ladner, MD. University of Kansas Medical Center, Kansas City, KS.

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