Iron overload in MDS—pathophysiology, diagnosis, and complications
- 12 October 2010
- journal article
- review article
- Published by Springer Nature in Annals of Hematology
- Vol. 90 (1) , 1-10
Abstract
Many patients with myelodysplastic syndromes (MDS) become dependent on blood transfusions and develop transfusional iron overload, which is exacerbated by increased absorption of dietary iron in response to ineffective erythropoiesis. However, it is uncertain whether there is an association among iron accumulation, clinical complications, and decreased likelihood of survival in MDS patients. Here, we discuss our current understanding of the effects of transfusion dependency and iron overload in MDS, indicate our knowledge gaps, and suggest that particular emphasis should be placed on further characterizing the role of redox-active forms of labile iron, which may be as important as the total iron burden.Keywords
This publication has 62 references indexed in Scilit:
- Identification of TWSG1 as a second novel erythroid regulator of hepcidin expression in murine and human cellsBlood, 2009
- Oxidative DNA damage in bone marrow cells of patients with low-risk myelodysplastic syndromeLeukemia Research, 2009
- Risk-adapted treatment of acute promyelocytic leukemia with all-trans retinoic acid and anthracycline monochemotherapy: long-term outcome of the LPA 99 multicenter study by the PETHEMA GroupBlood, 2008
- Urinary hepcidin excretion in patients with myelodysplastic syndrome and myelofibrosisBritish Journal of Haematology, 2008
- High levels of GDF15 in thalassemia suppress expression of the iron regulatory protein hepcidinNature Medicine, 2007
- Prognostic Factors and Life Expectancy in Myelodysplastic Syndromes Classified According to WHO Criteria: A Basis for Clinical Decision MakingJournal of Clinical Oncology, 2005
- LPI-labile plasma iron in iron overloadBest Practice & Research Clinical Haematology, 2005
- Hepcidin Regulates Cellular Iron Efflux by Binding to Ferroportin and Inducing Its InternalizationScience, 2004
- Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammationBlood, 2003
- Non‐Specific Serum Iron in Thalassaemia: an Abnormal Serum Iron Fraction of Potential ToxicityBritish Journal of Haematology, 1978