Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease

Author:

Weinstein David A.1,Roy Cindy N.1,Fleming Mark D.1,Loda Massimo F.1,Wolfsdorf Joseph I.1,Andrews Nancy C.1

Affiliation:

1. 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.

Abstract

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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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