Intact FGF23 and Markers of Iron Homeostasis, Inflammation, and Bone Mineral Metabolism in Acute Pediatric Infections
Eleni Papastergiou,
Dimitrios Rallis,
Afroditi Papagianni,
Vasileios Cholevas,
Nikolaos Katzilakis,
Ekaterini Siomou,
Eftichia Stiakaki,
Alexandros Makis
Affiliations
Eleni Papastergiou
Department of Pediatrics, University Hospital of Ioannina, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Dimitrios Rallis
Neonatal Intensive Care Unit, University Hospital of Ioannina, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Afroditi Papagianni
Laboratory of Child Health, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Vasileios Cholevas
Laboratory of Child Health, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Nikolaos Katzilakis
Department of Pediatric Hematology-Oncology, University Hospital of Heraklion, Postgraduate Program “Hematology-Oncology in Childhood and Adolescence” of Medical School, University of Crete, 71003 Heraklion, Greece
Ekaterini Siomou
Department of Pediatrics, University Hospital of Ioannina, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Eftichia Stiakaki
Department of Pediatric Hematology-Oncology, University Hospital of Heraklion, Postgraduate Program “Hematology-Oncology in Childhood and Adolescence” of Medical School, University of Crete, 71003 Heraklion, Greece
Alexandros Makis
Department of Pediatrics, University Hospital of Ioannina, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
We intend to evaluate the association of intact Fibroblast Growth Factor 23 (i-FGF23), a phosphaturic hormone that contributes to anemia of inflammation, with markers of iron homeostasis, inflammation, and bone mineral metabolism in acute pediatric infections. Seventy-nine children, aged 1 month–13 years, out of which forty-two were males and thirty-seven females, participated in this study. Children with diseases and nutrient deficiencies causing anemia were excluded. Twenty-six patients had bacterial infections, twenty-six had viral infections, and twenty-seven children served as healthy controls. Complete blood count, markers of inflammation, iron and mineral metabolism, serum hepcidin, and i-FGF23 were compared between the groups. Thirty-nine percent of patients with bacterial infection and twelve percent of patients with viral infection presented characteristics of anemia of inflammation (p p < 0.001). Hepcidin was significantly positively correlated with the duration of fever, markers of inflammation, and negatively with iron, mineral metabolism parameters, and i-FGF23. i-FGF23 was positively correlated with iron metabolism parameters and negatively with the duration of fever, markers of inflammation, and hepcidin. Hepcidin levels increase, whereas i-FGF23 levels decrease in acute pediatric infections. Further research is required to understand the role of FGF23 in the hepcidin–ferroportin axis and for hepcidin in the diagnosis of bacterial infections and mineral metabolism.
