Abstract

Introduction. Anemia is a frequent problem in hospitalized geriatric patients, and the anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the 2 most prevalent causes. The aim of the study was to assess the possible role of serum hepcidin in the differential diagnosis between ACD and IDA. Methods. We investigated serum hepcidin, iron status, anemia, and C-reactive protein in 39 consecutive geriatric patients with ACD and IDA. Serum hepcidin levels were determined using a commercial ELISA kit (DRG Instruments, Marburg, Germany). We also measured hepcidin in 26 healthy controls. Results. The serum hepcidin levels were not significantly higher in the 28 patients with ACD as compared to the 11 patients with IDA. Conclusions. The serum hepcidin levels measured using the commercial ELISA kit (DRG) do not appear to increase in older patients with ACD. It should be noted that an assay-specific problem could explain our results.

Highlights

  • Anemia is a frequent problem in hospitalized geriatric patients, and the anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the 2 most prevalent causes

  • An inflammatory process plays a central role in the pathogenesis of the ACD with low serum iron and normal or increased iron stores, while the absence of iron stores is the hallmark of the IDA [2]

  • It is remarkable that the serum hepcidin levels were comparable between the patients with IDA and ACD

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Summary

Introduction

Anemia is a frequent problem in hospitalized geriatric patients, and the anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the 2 most prevalent causes. The serum hepcidin levels measured using the commercial ELISA kit (DRG) do not appear to increase in older patients with ACD. The anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the 2 most prevalent causes of anemia in hospitalized geriatric patients [1]. Research on the pathogenesis of ACD has recently focused on the role of hepcidin, a 25 amino acid peptide synthesized in the liver and triggered by inflammatory stimulators such as interleukin-6 This peptide appears to be a key regulator of iron homeostasis [5]

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