Iron chelation beyond transfusion iron overload
Article first published online: 29 OCT 2007
Copyright © 2007 Wiley-Liss, Inc.
American Journal of Hematology
Volume 82, Issue S12, pages 1142–1146, December 2007
How to Cite
Pietrangelo, A. (2007), Iron chelation beyond transfusion iron overload. Am. J. Hematol., 82: 1142–1146. doi: 10.1002/ajh.21101
- Issue published online: 5 NOV 2007
- Article first published online: 29 OCT 2007
- Manuscript Received: 1 OCT 2007
- Manuscript Accepted: 1 OCT 2007
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.