Abstract
Iron status is the result of the balance between the rate of erythropoiesis and the amount of the iron stores. Direct consequence of an imbalance between the erythroid marrow iron requirements and the actual supply is a reduction of red cell hemoglobin content, which causes hypochromic mature red cells and reticulocytes. The diagnosis of iron deficiency is particularly challenging in patients with acute or chronic inflammatory conditions because most of the biochemical markers for iron metabolism (serum ferritin and transferrin ) are affected by acute phase reaction. For these reasons, interest has been generated in the use of erythrocyte and reticulocyte parameters, available on the modern hematology analyzers. Reported during blood analysis routinely performed on the instrument, these parameters can assist in early detection of clinical conditions (iron deficiency, absolute, or functional; ineffective erythropoiesis, including iron restricted or thalassemia), without additional cost. Technological progress has meant that in recent years modern analyzers report new parameters that provide further information from the traditional count. Nevertheless these new parameters are exclusive of each manufacturer, and they are patented. This is an update of these new laboratory test biomarkers of hypochromia reported by different manufactures, their meaning, and clinical utility on daily practice.
Highlights
Iron status is the result of the balance between the rate of erythropoiesis and the amount of the iron stores
The diagnosis of iron deficiency is challenging in patients with acute or chronic inflammatory conditions because most of the biochemical markers for iron metabolism are affected by acute phase reaction
The hormone controls the iron homeostasis and acts by inhibiting iron flows into plasma from macrophages involved in recycling of senescent erythrocytes, duodenal enterocytes engaged in the absorption of dietary iron, and hepatocytes that store iron [2]
Summary
The control of iron homeostasis acts at both the cellular and the systemic level and involves a complex system of different cell types, transporters, and signals. To maintain systemic iron homeostasis, communication between cells that absorb iron from the diet (duodenal enterocytes), consume iron (mainly erythroid precursors), and store iron (hepatocytes and tissue macrophages) must be tightly regulated [1]. The hormone controls the iron homeostasis and acts by inhibiting iron flows into plasma from macrophages involved in recycling of senescent erythrocytes, duodenal enterocytes engaged in the absorption of dietary iron, and hepatocytes that store iron [2]. Hepcidin reduces the quantity of circulating iron by limiting the egress of the metal from both intestinal and macrophage cells and is the key for the regulation of systemic iron homeostasis [3]
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