Iron deficiency with or without anemia often complicates inflammatory bowel disease by overt and/or occult gastrointestinal bleeding, such that regular monitoring is recommended.1 Moreover, while inflammatory bowel disease-induced impairment of iron absorption is rare due to the exclusive duodenal localization of the latter, high hepcidin induced changes in iron absorption and distribution may add another layer of complexity in patients with active inflammatory bowel disease emulgating into anemia of chronic disease.
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