Iron chelation beyond transfusion iron overload

Authors

  • Antonello Pietrangelo

    Corresponding author
    1. Center for Hemochromatosis, University Hospital of Modena and Reggio Emilia, Modena, Italy
    • Center for Hemochromatosis, University Hospital of Modena and Reggio Emilia, Policlinico, Via del Pozzo 71, 41100 Modena, Italy
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Abstract

The effects of systemic iron overload in hereditary (e.g., classic HFE hemochromatosis) or acquired disorders (e.g., transfusion-dependent iron overload) are well known. Several other iron overload diseases, with an observed mild-to-moderate increase in iron in selected organs (e.g., the liver or the brain), or with “misdistribution” of iron within cells (e.g., reticuloendothelial cells) or subcellular organelles (e.g., mitochondria), have been recognized more recently. The deleterious impact of any excess iron may be high as active redox iron may directly contribute to cell damage or affect signaling pathways involved in cell necrosis–apoptosis or organ fibrosis and cancer. This article discusses the potential use of iron chelation therapy to treat iron overload from causes other than transfusion overload. Am. J. Hematol., 2007. © 2007 Wiley-Liss, Inc.

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