Intact FGF23 and Markers of Iron Homeostasis, Inflammation, and Bone Mineral Metabolism in Acute Pediatric Infections

• Published in: Biology (Basel, Switzerland) Vol. 13; no. 9; p. 728
• Main Authors: Papastergiou, Eleni, Rallis, Dimitrios, Papagianni, Afroditi, Cholevas, Vasileios, Katzilakis, Nikolaos, Siomou, Ekaterini, Stiakaki, Eftichia, Makis, Alexandros
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01-09-2024
• Subjects: acute infection; Age; Anemia; anemia of inflammation; Antigens; Appendicitis; Bacteria; Bacterial infections; Blood; Bone growth; Children; Chronic kidney failure; Comorbidity; Deficiency diseases; Diseases; Erythropoiesis; Fever; Fibroblast growth factor 23; Fibroblast growth factors; functional iron deficiency; Greece; Health aspects; Heart rate; Hepcidin; Homeostasis; i-FGF23; Infections; Inflammation; Inflammatory diseases; Iron; Iron deficiency; Kidney diseases; Laboratories; Medical research; Medicine, Experimental; Metabolism; Patients; Pediatrics; Peptides; Physiological aspects; Polymerase chain reaction; Serology; Statistical analysis; Tumor necrosis factor-TNF; Viral infections; Vitamin deficiency; Greece; United States > US; anemia of inflammation; hepcidin; acute infection; functional iron deficiency; i-FGF23
• ISSN: 2079-7737; 2079-7737
• DOI: 10.3390/biology13090728

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 (
< 0.001). Ninety-two percent of patients with bacterial infection and eighty-one percent of patients with viral infection had functional iron deficiency (
< 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.