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P033. Serum hepcidin expression varies with disease activity in Crohn's disease

R. Chinnathuri1, D. Ward2, L. Nichols3, C. Tselepis2, T. Iqbal1, 1Queen ELizabeth Hospital, Gastroenterology Unit, Birmingham, United Kingdom, 2University of Birmingham, Cancer Studies, Birmingham, United Kingdom, 3University of Birmingham, Primary Care, Birmingham, United Kingdom


Hepcidin (Hp) is the “master regulator” of iron stores and key to the anaemia of chronic disease (ACD) [1]. ACD is common in Crohn's disease (CD) and there has been recent interest in the role of hepcidin both as a potential mediator of inflammation and anaemia in IBD [2]. In animal studies hepcidin has been implicated in the pathogenesis of IBD [3]. The aim of this pilot study was to investigate the expression of hepcidin in patients with CD and to relate this to disease activity (CRP) and anaemia (ferritin and haemoglobin Hb).


Serum samples from (12) patients with active CD (CDa) (CDAI >150) and (17) with inactive (CDi) were analysed for Hb, CRP, ferritin. Hp was measured in these and 48 “normal” controls (with GORD). Hp results were correlated with demographics, Hb, ferritin and CRP.


Hp was elevated in CDa (median 90 ng/ml) compared to CDi (32 ng/ml) and controls (44 ng/ml) (p < 0.001). CRP was also higher in Cda than Cdi (p = 0.003). Gender and age did not affect hepcidin expression. In the whole cohort Hp correlated positively with CRP (figure 1) and ferritin (figure 2). Hb correlated positively with ferritin. There was trend towards a negative association between Hb and Hp.

Figure 1. Hepcidin (ng/ml) vs CRP (ng/ml).

Figure 2. Hepcidin (ng/ml) vs ferritin (ng/ml).


In this study we have shown, for the first time that measuring serum hepcidin distinguished between patients with inactive and active CD. As expected hepcidin correlated with ferritin and CRP (both acute phase markers) but not with haemoglobin. These results would suggest that in the context of CD, inflammation rather than anaemia is the main trigger for hepcidin expression. This raises the intriguing possibility that hepcidin may promote anaemia perhaps by inhibiting iron uptake from the gut in active CD. This would be worthy of further investigation.

1. Andrews NC, (2008), Forging a field: the golden age of iron biology, Blood, 219–30.

2. Stein J, (2010), Diagnosis and management of iron deficiency anaemia in patients with IBD, Nat. Rev. Gastroenterol. Hepatol, 599–610.

3. Wang L, (2012), The bone morphogenetic protein-hepcidin axis as a therapuetic target in Inflammatory bowel disease. Inflamm. Bowel. Dis, 112–119.