after overnight fasting and again at specified timepoints after iron ingestion. The patients received one 30 mg iron tablet/capsule, and blood draws were performed after 60 and 120 min. After patients had consumed a very low-iron lunch (potato soup, bread), the same protocol was repeated. The area under the curve [AUC] for iron absorption at 60 and 120 min was calculated with regard to a.m./p.m. baselines. The blood samples were analyzed at Immundiagnostik AG, Bensheim, Germany, by LC/MS/MS. Results: Thirty patients with IBD were enrolled (17 f/13 m; 13 CD/17 UC; 37.6 6 13.6 y). Of these, 5/30(%) had inflammatory disease activity. The first administration of both ferrous sulphate and iron maltol led to a significant increase in plasma iron compared to baseline (P , 0.001), regardless of the presence of inflammation. After the second iron dose (p.m.), plasma iron fell insignificantly in both groups (P 5 0.011 and P 5 0.538, respectively, for the iron maltol and iron sulphate groups). Iron absorption capacity was higher in the iron maltol group in the morning, but did not differ after the second iron dose p.m. (P 5 0.280). Serum hepcidin values were significantly increased in both groups at afternoon baseline, i.e., prior to the second iron dose (P , 0.001), and serum hepcidin increase occurred independent of the type of iron. Conclusion(s): Hepcidin levels increased after intake of both ferrous sulphate and iron maltol, thus impairing iron absorption from the second daily dose. Intake of oral iron supplements by patients with IDA results in an acute increase of serum hepcidin levels over approximately 24 hours, regardless of whether ferric (III) or ferrous (II) iron is ingested and in spite of strong suppression of hepatic hepcidin expression due to iron deficiency and erythropoietic drive. Our data suggest that alternate day dosing of oral iron supplements may be appropriate in patients with IBD and anemia.