Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease
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.
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Microcytosis occurs in longstanding severe inflammation such as in Castleman disease, a lymphoproliferative disorder in which high IL-6 production strongly enhances hepcidin synthesis, or in patients with ectopic hepcidin expression by liver adenomas.
“Microcytosis occurs in longstanding severe inflammation such as in Castleman disease, a lymphoproliferative disorder in which high IL-6 production strongly enhances hepcidin synthesis103 or in patients with ectopic hepcidin expression by liver adenomas.104”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [104]
Hepcidin overexpression leads to low plasma iron levels (hypoferremia) and anemia.
“Hepcidin overexpression leads to low plasma iron levels (hypoferremia) and anemia (Weinstein et al., 2002; Roy et al., 2007; Theurl et al., 2009; Altamura et al., 2014).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Weinstein et al., 2002
Murine hepcidin mRNA is elevated in response to iron overload and decreased in response to iron deficiency.
“Initially, murine hepcidin mRNA was shown to be elevated in response to iron overload 92 and decreased in response to iron deficiency.99,100”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [100]
Patients with glycogen storage disease type 1a and hepatic adenomas develop anemia resembling anemia of chronic disease, the severity of which correlates directly with the extent of tumor burden.
“With Weinstein, Roy, and colleagues, we observed that these patients also develop anemia resembling the anemia of chronic disease, the severity of which correlates directly with the extent of tumor burden.100”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [100]
The hepatocyte-like cells of the adenomas expressed very high levels of hepcidin.
“We found that the hepatocytelike cells of the adenomas expressed very high levels of hepcidin 100 and speculated that our results could be generalized-that induction of hepcidin expression in response to inflammation might explain the anemia of chronic disease.”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [100]
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Transferrin is a major determinant of hepcidin expression in hypotransferrinemic mice
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Self-citationHepcidin: the Missing Link between Hemochromatosis andInfections
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Hepcidin and Ferroportin: The New Players in Iron Metabolism
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A dual-monoclonal sandwich ELISA specific for hepcidin-25
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“, 2010; Ganz and Nemeth, 2012), contributes to the development of anemia under inflammatory conditions (Weinstein et al., 2002; Kemna et al., 2005).”
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- Authors
- Weinstein, D. A., Roy, C. N., Fleming, M. D., Loda, M. F., Wolfsdorf, J. I., & Andrews, N. C.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2002-11-15
- Volume
- 100
- Issue
- 10
- Pages
- 3776-3781
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2073816425
- Cited by
- 632
- References
- 31
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 9 · 2023: 10 · 2022: 15 · 2021: 17 · 2020: 17 · 2019: 19 · 2018: 12 · 2017: 18 · 2016: 19 · 2015: 25 · 2014: 27 · 2013: 30 · 2012: 30
- FWCI
- 20.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- U.S. Public Health Service (K08-03600)
- National Heart, Lung, and Blood Institute (T32HL007623, T32-HL07623-15)
- National Center for Research Resources (M01-RR02172, M01RR002172)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Keywords
- hepcidin, anemia of chronic disease, hepatocellular adenoma, iron metabolism, erythropoiesis, iron absorption, liver transplantation
- MeSH terms
- Adolescent, Adult, Anemia, Refractory, Animals, Chronic Disease, Female, Glycogen Storage Disease Type I, Humans, Liver, Male, Mice, Mutant Strains, RNA, Messenger, RNA, Neoplasm, Up-Regulation, Adenoma, Liver Cell, Anemia, Iron-Deficiency, Antimicrobial Cationic Peptides, Mice, Hepcidins
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