Background: Hepcidin, a peptide produced by hepatocytes, regulates bodyiron homeostasis. Serum hepcidin is increased by inflammation and itsdetermination can be useful in the differential diagnosis of anemias duringinflammatory diseases.Methods: We measured serum hepcidin-25 and hepcidin-20 isoforms in 54patients with inflammatory bowel diseases (IBD) and 54 reference subjects(36 healthy controls and 18 anemic patients without inflammation or renalfailure). Disease activity, blood counts, iron status and erythropoiesis-relatedparameters were obtained for all study subjects.Results: In IBD hepcidin-25, the peptide bioactive isoform, correlatedpositively with C-reactive protein (CRP) and serum ferritin; an inversecorrelation was observed with transferrin, the soluble transferrin receptor(sTfR) and the sTfR/Log(ferritin) ratio. Similar correlations were found inreference subjects. Patients with anemia of inflammation had higher hepcidin-25 levels than those with iron deficiency anemia (IDA) or a combination of IDAand inflammation (P=0.0061). In patients with inflammation and serum ferritinconcentration 100 to 200 ng/mL hepcidin-25 was low, suggesting that thesepatients had iron deficiency. A serum hepcidin-25 concentration below 2.0 nMdifferentiated 85% of patients with IDA (with or without inflammation) frompatients with anemia of inflammation. In IBD hepcidin-20 correlated with bothhepcidin-25 and CRP.Conclusions: In IBD serum hepcidin-25 is influenced by iron stores,inflammation and iron requirement for erythropoiesis. Hepcidin-25determination can be useful in the differential diagnosis of IBD-associatedanemias. Serum hepcidin-20 is linked to hepcidin-25, but inflammation has anindependent regulatory role on its concentration, indicating that hepcidin-20may have a biological function.
Serum Hepcidin in Inflammatory Bowel Diseases: biological and clinical significance.
CAMPOSTRINI, Natascia;CORBELLA, Michela;GIRELLI, Domenico;
2013-01-01
Abstract
Background: Hepcidin, a peptide produced by hepatocytes, regulates bodyiron homeostasis. Serum hepcidin is increased by inflammation and itsdetermination can be useful in the differential diagnosis of anemias duringinflammatory diseases.Methods: We measured serum hepcidin-25 and hepcidin-20 isoforms in 54patients with inflammatory bowel diseases (IBD) and 54 reference subjects(36 healthy controls and 18 anemic patients without inflammation or renalfailure). Disease activity, blood counts, iron status and erythropoiesis-relatedparameters were obtained for all study subjects.Results: In IBD hepcidin-25, the peptide bioactive isoform, correlatedpositively with C-reactive protein (CRP) and serum ferritin; an inversecorrelation was observed with transferrin, the soluble transferrin receptor(sTfR) and the sTfR/Log(ferritin) ratio. Similar correlations were found inreference subjects. Patients with anemia of inflammation had higher hepcidin-25 levels than those with iron deficiency anemia (IDA) or a combination of IDAand inflammation (P=0.0061). In patients with inflammation and serum ferritinconcentration 100 to 200 ng/mL hepcidin-25 was low, suggesting that thesepatients had iron deficiency. A serum hepcidin-25 concentration below 2.0 nMdifferentiated 85% of patients with IDA (with or without inflammation) frompatients with anemia of inflammation. In IBD hepcidin-20 correlated with bothhepcidin-25 and CRP.Conclusions: In IBD serum hepcidin-25 is influenced by iron stores,inflammation and iron requirement for erythropoiesis. Hepcidin-25determination can be useful in the differential diagnosis of IBD-associatedanemias. Serum hepcidin-20 is linked to hepcidin-25, but inflammation has anindependent regulatory role on its concentration, indicating that hepcidin-20may have a biological function.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.