Iron deficiency leads to the suppression of hemoglobin (Hb) synthesis and induces metabolic disorders. In contrast, iron overload not only reduces the iron utilization efficiency but also induces oxidative stress. Iron metabolism in the body is closely regulated by hepcidin, a short peptide produced by the liver. Unfortunately, conventional iron indices may not always accurately reflect the iron status. For example, Hb concentration assessed using mature erythrocytes do not accurately reflect the real-time iron status due to their long lifespan. Reticulocytes are differentiated from erythroblasts after Hb synthesis and transform into mature erythrocytes in 1-2 days upon release into peripheral blood. Thus, Hb content in reticulocytes (Hb-ret) is more reflective of real-time Hb synthesis. Moreover, Hb-ret is affected only by the amount of iron intake as long as there is no hematopoietic disorder. Reticulocyte Hb content (CHr) can be accurately and inexpensively measured as Hb-ret by commercial H*3 or ADVIA hematology analyzers. CHr has been shown to be more effective than other indices of iron metabolism for the diagnosis of iron deficiency, for early detection of the therapeutic effects of iron therapy, and for differentiation of the beta thalassemia trait.
Keywords: Anemia of chronic disease; Chronic kidney disease; Iron deficiency; Reticulocyte hemoglobin content; Thalassemia trait.
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