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Blood, 21 May 2009, Vol. 113, No. 21, pp. 5277-5286. Prepublished online as a Blood First Edition Paper on March 17, 2009; DOI 10.1182/blood-2008-12-195651. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2008-12-195651v1 113/21/5277    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 Google Scholar Articles by Theurl, I. Articles by Weiss, G. PubMed PubMed Citation Articles by Theurl, I. Articles by Weiss, G. Related Collections Free Research Articles Red Cells, Iron, and Erythropoiesis Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS, IRON, AND ERYTHROPOIESIS Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications Igor Theurl1, Elmar Aigner2, Milan Theurl1,3, Manfred Nairz1, Markus Seifert1, Andrea Schroll1, Thomas Sonnweber1, Lukas Eberwein1, Derrick R. Witcher4, Anthony T. Murphy4, Victor J. Wroblewski4, Eva Wurz1, Christian Datz2, and Guenter Weiss1 1 Department of Internal Medicine I, Clinical Immunology and Infectious Diseases, Medical University of Innsbruck, Innsbruck, Austria; 2 Department of Internal Medicine, General Hospital Oberndorf, Oberndorf, Austria; 3 Department of Ophthalmology, Medical University of Innsbruck, Innsbruck, Austria; and 4 Biotechnology Discovery Research, Lilly Research Laboratories, Indianapolis, IN The anemia of chronic disease (ACD) is characterized by macrophage iron retention induced by cytokines and the master regulator hepcidin. Hepcidin controls cellular iron efflux on binding to the iron export protein ferroportin. Many patients, however, present with both ACD and iron deficiency anemia (ACD/IDA), the latter resulting from chronic blood loss. We used a rat model of ACD resulting from chronic arthritis and mimicked ACD/IDA by additional phlebotomy to define differing iron-regulatory pathways. Iron retention during inflammation occurs in macrophages and the spleen, but not in the liver. In rats and humans with ACD, serum hepcidin concentrations are elevated, which is paralleled by reduced duodenal and macrophage expression of ferroportin. Individuals with ACD/IDA have significantly lower hepcidin levels than ACD subjects, and ACD/IDA persons, in contrast to ACD subjects, were able to absorb dietary iron from the gut and to mobilize iron from macrophages. Circulating hepcidin levels affect iron traffic in ACD and ACD/IDA and are more responsive to the erythropoietic demands for iron than to inflammation. Hepcidin determination may aid to differentiate between ACD and ACD/IDA and in selecting appropriate therapy for these patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. B. Keel and J. L. Abkowitz The Microcytic Red Cell and the Anemia of Inflammation N. Engl. J. Med., November 5, 2009; 361(19): 1904 - 1906. [Full Text] [PDF]

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