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Patients with inflammatory bowel disease (IBD) commonly develop iron deficiency and, if left untreated, they can develop iron deficiency anemia (IDA). In IBD, IDA is caused mainly by blood loss and/or impaired iron absorption from the gut,1 as well as by reduced iron availability for erythropoiesis.2 Under inflammatory conditions, iron sequestration is induced by an increased expression of hepcidin, which binds to and leads to degradation of the iron-export protein ferroportin and thus inhibits the release of iron from the enterocytes and from the macrophages of the reticuloendothelial system. As a consequence, the absorption and availability of iron is decreased.3 Oral iron, usually in the form of ferrous sulfate (FS) or ferrous fumarate (FF), is recommended as firstline therapy for IDA in IBD in some guidelines,4 although intravenous iron therapy is recommended as a preferred treatment option in other guidelines5 and in a number of recent publications.6–8