Background: Hepcidin-25 is a liver-derived key peptide hormone that regulates iron homeostasis in humans. Recent studies have suggested that hepcidin also play a key role in host-defense mechanism. Iron is essential for the survival and growth of bacteria. When the bacteria infect macrophages, macrophages release a number of cytokines including interleukin-6, which increase production of hepcidin in the hepatocytes. This up-regulation of hepcidin leads to iron depletion and inhibition of bacterial growth. The aim of this study is to investigate serum hepcidin-25 levels and their relationship with the severity of inflammation and bacteremia in patients with systemic inflammatory response syndrome (SIRS).

Methods: Of all patients who were admitted to our department of general medicine between August 1, 2015 and August 31, 2017, 113 consecutive patients (aged 63.4±21, male 50, female 63) with 2 or more SIRS criteria were enrolled. We measured complete blood cell count, hepcidin-25, iron, iron-binding capacity, ferritin, blood urea nitrogen, creatinine, albumin, and C-reactive protein at day 1, 2 and 3 after admission. The patients were divided into 3 groups for comparison: Bacteremia group (27 patients), Bacterial infection with negative blood culture group (60 patients), and Non-bacterial infection group (26 patients).

Results: Hepcidin-25 levels on day1 were 167±120 in patients with 2 criteria, 190±97 in those with 3, and 211±100 ng/ml in those with 4, respectively (P=0.442). There was significant difference in the maximum hepcidin-25 levels between the bacteremia group, the bacterial infection with negative blood cultures group, and the non-bacterial group (252±122 vs 187±99 vs 175±132 ng/ml, P<0.05). The hepcidin-25 levels of the bacteremia group were significantly higher than those of the other groups.

Conclusions: Our findings suggest that serum hepcidin-25 levels have not significant impact on the severity of inflammation, but that they may contribute to determining bacteremia in SIRS patients.