“…It is considered that ID in HF partially results from inadequate iron intake in the diet [19, 20], low bioavailability of iron in the diet (more frequent in developing countries), and handicapped gastrointestinal absorption. The latter results from intestinal interstitial oedema, the use of medications increasing gastric pH (such as proton pump inhibitors or H 2 receptor antagonists), and the ingestion of food reducing iron absorption (calcium, tannins, oxalates, phytate, phosphates, antiacids) [21, 22].…”