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Iron deficiency in critically ill patients: highlighting the role of hepcidin

Critical Care
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/cc9992
  • Review
  • Biology
  • Medicine


CC9992-Heming.indd Introduction Iron is a paradoxical element, essential for living organ- isms but also potentially toxic. Indeed, iron has the ability to readily accept and donate electrons, interconverting from soluble ferrous form (Fe2+) to the insoluble ferric form (Fe3+). Th is capacity allows iron to play a major role in oxygen transport (as the central part of hemoglobin) but also in electron transfer, nitrogen fi xation or DNA synthesis, all essential reactions for living organisms. Indeed, iron defi ciency is the main cause of anemia [1] as well as a cause of fatigue [2,3] and decreased eff ort capacity [4,5]. However, despite a high frequency of anemia among critically ill patients, with 60 to 66% being anemic at intensive care unit (ICU) admission [6,7], to date little is known about iron defi ciency and iron metabolism in critically ill patients [8]. Th e interaction between infl ammation and iron metabolism interferes with the usual iron metabolism variables and renders this metabolism diffi cult to investigate [9,10]. Th e recent discovery of hepcidin (the master regulator of iron metabolism) has shed new light on the regulation of iron homeostasis and has helped our understanding of complex clinical situations, such as those observed in critically ill patients, where several regulatory circuits inter fere with iron metabolism [11]. Th e purpose of this article is to review iron metabolism and anemia in critically ill patients as well as the role of hepcidin, and to discuss the indications for iron supplementation in these patients. Iron metabolism overview and the role of hepcidin Although iron is essential for life, it may also be toxic because of its capacity to react with oxygen and to promote the production of free radicals. Th is duality is found in human pathology: Iron defi ciency (because of poor iron intake, abnormal blood losses etc...) presents with anemia and fatigue; whereas iron overload (mainly in hereditary hemochromatosis

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