P139. Serum hepcidin levels predict intestinal iron absorption in IBD patients
M. Wiesenthal1, A. Dignass2, F. Hartmann1, T. Iqbal3, J. Stein1, 1Crohn Colitis Center, DGD Krankenhaus Sachsenhausen, Frankfurt, Germany, 2Agaplesion Markus Hospital, Department of Medicine I, Frankfurt, Germany, 3Gastroenterology Unit, Queen Elizabeth Hospital, Birmingham, United Kingdom
Circulating hepcidin is proposed to regulate iron absorption by modulating iron export by ferroportin at the basolateral membrane of the duodenal mucosal cells and/or uptake into the cells at the apical membrane by DMT1. To date, no data have shown a relationship between plasma hepcidin concentrations and iron absorption in IBD patients. In the present study, we used stored samples from a human iron absorption study to further test the hypothesis that plasma hepcidin may explain interindividual variation in iron absorption in IBD patients.
Serum ferritin (SF) and serum markers of inflammation [high-sensitivity C-reactive protein (hsCRP) and IL-6] were measured in stored samples from a human iron absorption study using commercially available immune-assays. Hepcidin-25 concentrations were determined in fasting samples from 71 adult subjects with IBD (31 UC, 40 CD) and 26 healthy controls. Hepcidin was measured by LC-MS.
There was a positive correlation between hepcidin (mean: 2.3; range: 0.1–7.8nmol/L) and hsCRP (p < 0.005), but not between hepcidin and serum ferritin (p > 0.05). Whereas iron absorption was negatively correlated with serum ferritin only in patients with inactive disease (hsCRP <5md/dl; p < 0.001), a negative correlation was observed with serum hepcidin in both active and inactive disease (p = 0.006), independent of IBD phenotype. Multiple linear regression models showed that serum hepcidin in isolation significantly predicted the interindividual variation in iron absorption.
Concentration of serum hepcidin, but not serum ferritin, was highly correlated with intestinal iron absorption in IBD patients.