Hepcidin concentrations in serum and urine correlate with iron homeostasis in preterm infants.

Abstract

To evaluate whether hepcidin concentrations in serum (Hep((S))) and urine (Hep((U))) correlate with iron metabolism, erythropoiesis, and inflammation in preterm infants. Thirty-one preterm infants (23-32 weeks gestational age) were included. The concentration of the mature, 25 amino-acid form of hepcidin was determined by enzyme-linked immunosorbent assay in serum, urine, blood counts, reticulocytes, and iron measurements. Median (IQR) Hep((S)) was 52.4 (27.9-91.9) ng/mL. The highest values were measured in patients with systemic inflammation. Hep((S)) and Hep((U)) correlated strongly (P = .0007). Hep((S)) and Hep((U)) also correlated positively with ferritin (P = .005 and P = .0002) and with reticulocyte hemoglobin content (P = .015 and P = .015). Hep((S)) and Hep((U)) correlated negatively with soluble transferrin receptor/ferritin-ratio (P = .005 and P = .003). Infants with lower hemoglobin concentrations and higher reticulocyte counts had lower Hep((S)) (P = .0016 and P = .0089). In sick preterm infants, iron status, erythropoiesis, anemia, and inflammation correlated with the mature 25 amino-acid form of hepcidin. Further evaluation of Hep((U)) for non-invasive monitoring of iron status in preterm infants appears justified.