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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2002-04-1260. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-04-1260v1 100/10/3776    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 Weinstein, D. A. Articles by Andrews, N. C. Search for Related Content PubMed PubMed Citation Articles by Weinstein, D. A. Articles by Andrews, N. C. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2002, Vol. 100, No. 10, pp. 3776-3781 RED CELLS Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease David A. Weinstein, Cindy N. Roy, Mark D. Fleming, Massimo F. Loda, Joseph I. Wolfsdorf, and Nancy C. Andrews From Children's Hospital, Harvard Medical School; Brigham and Women's Hospital and Harvard Medical School; Dana-Farber Cancer Institute; and Howard Hughes Medical Institute, Children's Hospital, Harvard Medical School; all of Boston, MA. The anemia of chronic disease is a prevalent, poorly understood condition that afflicts patients with a wide variety of diseases, including infections, malignancies, and rheumatologic disorders. It is characterized by a blunted erythropoietin response by erythroid precursors, decreased red blood cell survival, and a defect in iron absorption and macrophage iron retention, which interrupts iron delivery to erythroid precursor cells. We noted that patients with large hepatic adenomas had severe iron refractory anemia similar to that observed in anemia of chronic disease. This anemia resolved spontaneously after adenoma resection or liver transplantation. We investigated the role of the adenomas in the pathogenesis of the anemia and found that they produce inappropriately high levels of hepcidin mRNA. Hepcidin is a peptide hormone that has been implicated in controlling the release of iron from cells. We conclude that hepcidin plays a major, causative role in the anemia observed in our subgroup of patients with hepatic adenomas, and we speculate that it is important in the pathogenesis of the anemia of chronic disease in general. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. A. Melis, M. Cau, R. Congiu, G. Sole, S. Barella, A. Cao, M. Westerman, M. Cazzola, and R. Galanello A mutation in the TMPRSS6 gene, encoding a transmembrane serine protease that suppresses hepcidin production, in familial iron deficiency anemia refractory to oral iron Haematologica, October 1, 2008; 93(10): 1473 - 1479. [Abstract] [Full Text] [PDF] N. C. Andrews Forging a field: the golden age of iron biology Blood, July 15, 2008; 112(2): 219 - 230. [Full Text] [PDF] Q. Xu, C.-H. C. Cheng, P. Hu, H. Ye, Z. Chen, L. Cao, L. Chen, Y. Shen, and L. 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