BACKGROUND: Biochemical markers have problems in distinguishing iron deficiency anemia (IDA) from anemia of chronic disease (ACD), and the combined state of iron-restricted erythropoiesis (IRE) with ACD (ACD/IRE). We investigated the extent to which hepcidin-25, a potential marker for the evaluation of iron metabolism, enables the differentiation of the states above, and to assess its correlation with convential markers of iron deficiency. METHODS: One hundred and fifty-five patients with anemia were classified as having IDA, ACD or ACD/IRE using clinical findings, biochemical markers and hematological indices. The diagnostic performance of hepcidin-25 alone or in combination with the reticulocyte hemoglobin content (CHr) was evaluated using receiver-operating characteristic curve analysis and multivariate analysis. Hepcidin-25 was determined using an isotope-dilution micro-HPLC-tandem mass spectrometry method. RESULTS: Hepcidin-25 correlated with biochemical markers of iron deficiency but not with hematological indices. Use of a hepcidin-25 cut-off of ≤ 4 nmol/L allowed the differentiation of IDA from ACD and ACD/IRE, but not the discrimination of ACD from ACD/IRE in patients with severe inflammation. Furthermore, the discrimination of ACD/IRE from ACD required the combination with CHr. CONCLUSIONS: Hepcidin-25 is primarily an indicator for decreased body iron levels, but not for IRE. The combination of hepcidin-25 with CHr in a diagnostic plot (hepcidin-25 plot) might be useful for the differentiation of ACD from ACD/IRE and IDA.
BACKGROUND: Biochemical markers have problems in distinguishing iron deficiency anemia (IDA) from anemia of chronic disease (ACD), and the combined state of iron-restricted erythropoiesis (IRE) with ACD (ACD/IRE). We investigated the extent to which hepcidin-25, a potential marker for the evaluation of iron metabolism, enables the differentiation of the states above, and to assess its correlation with convential markers of iron deficiency. METHODS: One hundred and fifty-five patients with anemia were classified as having IDA, ACD or ACD/IRE using clinical findings, biochemical markers and hematological indices. The diagnostic performance of hepcidin-25 alone or in combination with the reticulocyte hemoglobin content (CHr) was evaluated using receiver-operating characteristic curve analysis and multivariate analysis. Hepcidin-25 was determined using an isotope-dilution micro-HPLC-tandem mass spectrometry method. RESULTS: Hepcidin-25 correlated with biochemical markers of iron deficiency but not with hematological indices. Use of a hepcidin-25 cut-off of ≤ 4 nmol/L allowed the differentiation of IDA from ACD and ACD/IRE, but not the discrimination of ACD from ACD/IRE in patients with severe inflammation. Furthermore, the discrimination of ACD/IRE from ACD required the combination with CHr. CONCLUSIONS: Hepcidin-25 is primarily an indicator for decreased body iron levels, but not for IRE. The combination of hepcidin-25 with CHr in a diagnostic plot (hepcidin-25 plot) might be useful for the differentiation of ACD from ACD/IRE and IDA.