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Hepcidin, interleukin-6 and hematological iron markers in males before and after heart surgery
- Hoppe, Michael, Lönnerdal, Bo, Hossain, Bakhtiar, Olsson, Sigvard, Nilsson, Folke, Lundberg, Per-Arne, Rödjer, Stig, Hulthén, Lena
- Journal of nutritional biochemistry 2009 v.20 no.1 pp. 11-16
- men, surgery, heart, heart diseases, postoperative care, postoperative complications, iron deficiency anemia, blood serum, interleukin-6, inflammation, biomarkers, hemoglobin, iron absorption, C-reactive protein, ferritin, transferrin, nutritional status
- Anemia of inflammation in patients with acute or chronic acute-phase activation is a common clinical problem. Hepcidin is a peptide shown to be the principal regulator of the absorption and systemic distribution of iron. Main inducers of hepcidin are iron overload, hypoxia and inflammation, where the latter has been linked to hepcidin via increased interleukin-6 (IL-6). This article addresses the impact and time course of postoperative acute-phase reaction in humans following heart surgery on prohepcidin, hepcidin, hematological markers and IL-6 concentrations. Serum concentrations of prohepcidin, hepcidin, IL-6 and hematological iron parameters were studied in five male patients without infection before and after heart surgery. This study, which is the first to report the impact on serum hepcidin and serum prohepcidin concentrations in patients following surgery, clearly demonstrates the induction of hypoferremia due to the postoperative acute-phase reaction. Significant changes were seen for serum iron concentration, transferrin saturation, total iron binding capacity and hemoglobin concentration. A significant increase in ferritin concentration was seen 96-144 h postoperatively. Additionally, there were significant alterations in both serum hepcidin after 96-144 h and serum prohepcidin after 48 h compared with preoperative values. Serum prohepcidin decreased, whereas serum hepcidin increased. In conclusion, changes in serum prohepcidin were followed by an increase in serum hepcidin. This speaks in favor of a chain of action where proteolytic trimming of serum prohepcidin results in increased serum hepcidin. However, hypoferremia appeared prior to the changes in serum prohepcidin and serum hepcidin.