Anemia is the most common extraintestinal complication in patients with inflammatory bowel disease. It is so frequent that it is indispensable to perform periodic analytical controls for early detection and treatment. The mechanisms that generate it could be diverse, being iron deficiency (genuine or functional) the most common, followed by and usually associated with chronic inflammation. We evaluated these mechanisms, esentially with ferritin, transferrin saturation and inflammatory markers. A low transferrin saturation indicated iron deficiency, “genuine” if ferric deposits are also low, or “functional” if they are normal or even high. Iron deposits are not easily assessed because their usual marker, ferritin, is substantially influenced by the existence of an inflammation. This is not always easy to estimate either, usually it is evaluated with the CRP. We consider iron deposits are diminished if ferritin is < 30 μg/l without inflammation, and < 100 μg/l when inflammation is present. Other parameters less influenced by inflammation could be useful to discriminate between both types of anemia. Endovenous iron, essential in some situations, is increasingly recommended versus the oral treatment because it avoids the adverse gastrointestinal effects, it is safe, efficient and faster. It is also very convenient for the patient if new formulas are being used, since they can administer all necessary iron in only 1 or 2 doses. The goal of this treatment is to bring hemoglobin back to normal levels, and ideally reach a ferritin of > 400 μg/l, thus reducing the elevated risk of recurrence of anemia. Once corrected, periodic controls must be conducted, at least quarterly during the first year.
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