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* = Presenting author

P032. Serum hepcidin in inflammatory bowel diseases

A. Di Sabatino1, G. Bergamaschi1, R. Albertini1, F. Costanzo1, M. Guerci1, M. Masotti1, A. Pasini1, P. Giuffrida1, P. Biancheri1, N. Campostrini2, M. Corbella2, D. Girelli2, G.R. Corazza1, 1IRCCS Policlinico San Matteo, Pavia, Italy, 2Department of Medicine, Verona, Italy

Background

Hepcidin, a small peptide hormone mainly produced by hepatocytes, regulates iron homeostasis acting as a negative mediator of iron absorption and of iron release from tissue stores. Stimulation of hepcidin production during inflammation has a causal role in the pathogenesis of the anemia of inflammation.

Methods

We determined serum hepcidin concentration in 54 patients with inflammatory bowel diseases (IBD) and in a group of 25 reference subjects (12 healthy controls and 13 patients with anemia not associated with inflammation or renal failure). Complete blood counts, iron status, erythropoiesis-related parameters and disease activity were evaluated in addition to hepcidin.

Results

In IBD hepcidin concentration positively correlated with C-reactive protein and serum ferritin, whereas an inverse correlation was observed with transferrin concentration, the soluble transferrin receptor (sTfR) and the sTfR/Log (ferritin) ratio. Hepcidin levels were higher in patients with active disease than in those with quiescent disease (6.68±9.62 nM and 2.61±3.11 nM respectively, p = 0.0419). 26 IBD patients had anemia. No differences in hepcidin levels were found between anemic and non-anemic subjects; however, serum hepcidin was lower in patients with iron deficiency anemia (IDA) and in those with a combination of IDA and anemia of inflammation than in patients with isolated anemia of inflammation (1.55±3.00 nM, 3.59±5.64 nM and 14.77±13.90 nM respectively, p = 0.0229). A serum hepcidin concentration below 2.0 nM correctly differentiated 85% of patients with IDA (with or without inflammation) from patients with anemia of inflammation. Patients with inflammation and serum ferritin concentrations 100 to 200 ng/mL had low hepcidin levels, suggesting that during inflammation iron deficiency can associate with serum ferritin concentrations up to 200 ng/mL.

Conclusion

Our results show that in IBD serum hepcidin concentration is influenced by iron stores, iron requirements for erythropoiesis and inflammation. Hepcidin determination can be useful in the differential diagnosis of IBD-associated anemias.