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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4527-4531. Prepublished online as a Blood First Edition Paper on January 25, 2005; DOI 10.1182/blood-2004-09-3468. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-09-3468v1 105/11/4527    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Le Lan, C. Articles by Brissot, P. Search for Related Content PubMed PubMed Citation Articles by Le Lan, C. Articles by Brissot, P. Related Collections Red Cells Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Redox active plasma iron in C282Y/C282Y hemochromatosis Caroline Le Lan, Olivier Loréal, Tally Cohen, Martine Ropert, Hava Glickstein, Fabrice Lainé, Michel Pouchard, Yves Deugnier, André Le Treut, William Breuer, Z. Ioav Cabantchik, and Pierre Brissot From the Service des Maladies du Foie and INSERM U-522 and the Laboratoire de Biochimie Générale et Enzymologie, University Hospital Pontchaillou, and the Centre d'examen de Santé CPAM, Rennes, France; and the Department of Biological Chemistry, Institute of Life Sciences, Hebrew University of Jerusalem, Israel. Labile plasma iron (LPI) represents the redox active component of non–transferrin-bound iron (NTBI). Its presence in thalassemic patients has been recently reported. The aim of the present study was to quantify LPI in HFE genetic hemochromatosis (GH) and to characterize the mechanisms accounting for its appearance. We studied 159 subjects subdivided into the following groups: (1) 23 with iron overloaded GH; (2) 14 with iron-depleted GH; (3) 26 with dysmetabolic hepatosiderosis; (4) 33 with alcoholic cirrhosis; (5) 63 healthy controls. Both NTBI and LPI were substantially higher in patients with iron-overloaded GH than in those with iron-depleted GH or in healthy controls. LPI was significantly correlated with serum transaminase increase in this group. LPI was elevated in the alcoholic cirrhosis subgroup of severely affected patients. LPI was found essentially when transferrin saturation exceeded 75%, regardless of the etiologic condition. Transferrin saturation above 75% was related to iron overload in GH and to liver failure in alcoholic cirrhosis. LPI is present in C282Y/C282Y hemochromatosis and may be a marker of toxicity due to its potential for catalyzing the generation of reactive oxygen radicals in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D.-H. Lee, D. Y. Liu, D. R. Jacobs Jr., H.-R. Shin, K. Song, I.-K. Lee, B. Kim, and R. C. Hider Common Presence of Non-Transferrin-Bound Iron Among Patients With Type 2 Diabetes Diabetes Care, May 1, 2006; 29(5): 1090 - 1095. [Abstract] [Full Text] [PDF] P. Brissot and F. de Bels Current Approaches to the Management of Hemochromatosis Hematology, January 1, 2006; 2006(1): 36 - 41. [Abstract] [Full Text] [PDF]

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