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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 (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 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 Theurl, I. Articles by Weiss, G. Search for Related Content PubMed PubMed Citation Articles by Theurl, I. Articles by Weiss, G. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 19, 2008 Accepted March 3, 2009 Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications Igor Theurl, Elmar Aigner, Milan Theurl, Manfred Nairz, Markus Seifert, Andrea Schroll, Thomas Sonnweber, Lukas Eberwein, Derrick R. Witcher, Anthony T. Murphy, Victor J. Wroblewski, Eva Wurz, Christian Datz, and Guenter Weiss* Department of Internal Medicine I, Clinical Immunology and Infectious Diseases, Medical University of Innsbruck, Innsbruck, Austria General Hospital Oberndorf, Department of Internal Medicine, Oberndorf, Austria Department of Ophthalmology, Medical University of Innsbruck, Innsbruck, Austria Biotechnology Discovery Research, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, United States * Corresponding author; email: guenter.weiss{at}i-med.ac.at. 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 upon binding to the iron export protein ferroportin. Many patients, however, present with both, ACD and iron deficiency anemia (ACD/IDA), the later due to chronic blood loss. We used a rat model of ACD due to chronic arthritis and mimicked ACD/IDA by additional phlebotomy in order 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 suffering from ACD, serum hepcidin concentrations are elevated, which is paralleled by reduced duodenal and macrophage expression of ferroportin. Individuals suffering from ACD/IDA have significantly lower hepcidin levels than ACD subjects, and ACD/IDA individuals, 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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