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(Stroke. 2009;40:S90.)
© 2009 American Heart Association, Inc.
Brain Hemorrhage |
From Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.
Correspondence to Magdy Selim, MD, PhD, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215. E-mail mselim{at}bidmc.harvard.edu
Iron resulting from hemoglobin degradation is linked to delayed neuronal injury after intracerebral hemorrhage. Extensive preclinical investigations indicate that the iron chelator, deferoxamine mesylate, is effective in limiting hemoglobin- and iron-mediated neurotoxicity. However, clinical studies evaluating the use of deferoxamine in intracerebral hemorrhage are shortcoming. This article reviews the potential role of deferoxamine as a promising neuroprotective agent to target the secondary effects of intracerebral hemorrhage to limit brain injury and improve outcome, and ongoing efforts to translate the preclinical findings into clinical investigations.
Key Words: deferoxamine ICH edema neuroprotection
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