title: Serum hepcidin in inflammatory bowel diseases: biological and clinical significance.
abstract: BACKGROUND
  Hepcidin, a peptide produced by hepatocytes, regulates body iron homeostasis. Inflammation increases serum hepcidin, and its determination can be useful in the differential diagnosis of anemias during inflammatory diseases.
  
  
  METHODS
  We measured serum hepcidin-25 and hepcidin-20 isoforms in 54 patients with inflammatory bowel diseases (IBD) and 54 reference subjects (36 healthy controls and 18 anemic patients without inflammation or renal failure). Disease activity, blood counts, iron status, and erythropoiesis-related parameters were obtained for all study subjects.
  
  
  RESULTS
  In IBD hepcidin-25, the peptide bioactive isoform correlated positively with C-reactive protein and serum ferritin; an inverse correlation was observed with transferrin, the soluble transferrin receptor, and the soluble transferrin receptor to Log(ferritin) ratio. Similar correlations were found in reference subjects. Patients with anemia of inflammation had higher hepcidin-25 levels than those with iron deficiency anemia or a combination of iron deficiency anemia and inflammation (P = 0.0061). In patients with inflammation and serum ferritin concentration 100 to 200 ng/mL, hepcidin-25 was low, suggesting that these patients had iron deficiency. A serum hepcidin-25 concentration below 2.0 nM differentiated 85% of patients with iron deficiency anemia (with or without inflammation) from patients with anemia of inflammation. In IBD, hepcidin-20 correlated with both hepcidin-25 and C-reactive protein.
  
  
  CONCLUSIONS
  In IBD, iron stores, inflammation, and iron requirement for erythropoiesis influence serum hepcidin-25. Hepcidin-25 determination can be useful in the differential diagnosis of IBD-associated anemias. Serum hepcidin-20 is linked to hepcidin-25, but inflammation has an independent regulatory role on its concentration, indicating that hepcidin-20 may have a biological function.
authors.affiliation: Department of Internal Medicine, University of Pavia Medical School and Fondazione IRCCS Policlinico San Matteo, Pavia, Italy. n.bergamaschi@smatteo.pv.it
authors.forename: Gaetano
authors.initials: G
authors.lastname: Bergamaschi
authors.forename: Antonio
authors.initials: A
authors.lastname: Di Sabatino
authors.forename: Riccardo
authors.initials: R
authors.lastname: Albertini
authors.forename: Filippo
authors.initials: F
authors.lastname: Costanzo
authors.forename: Marco
authors.initials: M
authors.lastname: Guerci
authors.forename: Michela
authors.initials: M
authors.lastname: Masotti
authors.forename: Alessandra
authors.initials: A
authors.lastname: Pasini
authors.forename: Alessandro
authors.initials: A
authors.lastname: Massari
authors.forename: Natascia
authors.initials: N
authors.lastname: Campostrini
authors.forename: Michela
authors.initials: M
authors.lastname: Corbella
authors.forename: Domenico
authors.initials: D
authors.lastname: Girelli
authors.forename: Gino Roberto
authors.initials: GR
authors.lastname: Corazza
mesh_terms: D000328:Adult; D000740:Anemia / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D015415:Biomarkers / Q000097:blood*; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000097:blood / Q000150:complications*; D003424:Crohn Disease / Q000097:blood / Q000150:complications*; D005260:Female; D005500:Follow-Up Studies; D064451:Hepcidins / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D015415:Biomarkers; D064451:Hepcidins