However , in patients with IBD flares and inadequate responses to or side effects with oral preparations , intravenous iron supplementation is the therapy of choice .
Neither oral nor intravenous therapy seems to exacerbate the clinical course of IBD , and intravenous iron therapy can be administered even in active disease stages and concomitantly with biologics .
Based on the data presented , oral iron therapy should be preferred for patients with quiescent disease stages and trivial iron deficiency  anemia unless such patients are intolerant or have an inadequate response , whereas intravenous iron supplementation may be of advantage in patients with aggravated anemia or flares of IBD because inflammation hampers intestinal absorption of iron
Abstract Anemia is the most frequent complication of inflammatory bowel disease ( IBD ) , but anemia , mostly due to iron deficiency , has long been neglected in these patients .
The aim was to briefly present the pathophysiology , followed by a balanced overview of the different forms of iron replacement available , and subsequently , to perform a systematic review of studies performed in the last decade on the treatment of iron-deficiency anemia in IBD .
Hepcidin levels predict nonresponsiveness to oral iron therapy in patients with iron deficiency anemia
Levels of hepcidin , a major regulator of iron homeostasis , may identify patients with iron deficiency anemia ( IDA ) who will not respond to oral iron therapy . In this study , IDA patients underwent a 14‐day trial ( run‐in ) course of ferrous sulfate therapy . Nonresponders ( Hgb increase < 1 g/dL with 67 % compliance rate ) were r and omized to IV ferric carboxymaltose ( FCM ; two injections of 750 mg ) or further oral iron for 14 days . Screening hepcidin levels were 38.4 versus 11.3 ng/mL , P = 0.0002 in nonresponders versus responders to a trial of oral iron . Hepcidin of > 20 ng/mL , showed sensitivity of 41.3 % , specificity of 84.4 % , and positive predictive value of 81.6 % for predicting nonresponsiveness to oral iron . PPVs for ferritin > 30 ng/mL or transferrin saturation (TSAT)>15 % were 59.2 and 55 % , respectively . Negative predictive values for hepcidin , ferritin , and TSAT were 46.3 , 22.7 , and 19.7 , respectively . FCM versus oral iron showed Hgb increases of ≥1 gm/dL in 65.3 % versus 20.8 % ( P < 0.0001 ) and Hgb increases of 1.7 ± 1.3 versus 0.6 ± 0.9 g/dL ( P = 0.0025 ) , respectively . We conclude that hepcidin predicts nonresponsiveness to oral iron in patients with IDA and is superior to TSAT or ferritin for this purpose . Nonresponse  to oral iron therapy does not rule out IDA , since two‐thirds of patients subsequently responded to intravenous iron . Am . J. Hematol . 88:97–101 , 2013 . © 2012 Wiley Periodicals ,
However , in patients with IBD flares and inadequate responses to or side effects with oral preparations , intravenous iron supplementation is the therapy of choice .
Neither oral nor intravenous therapy seems to exacerbate the clinical course of IBD , and intravenous iron therapy can be administered even in active disease stages and concomitantly with biologics .
Based on the data presented , oral iron therapy should be preferred for patients with quiescent disease stages and trivial iron deficiency  anemia unless such patients are intolerant or have an inadequate response , whereas intravenous iron supplementation may be of advantage in patients with aggravated anemia or flares of IBD because inflammation hampers intestinal absorption of iron
Abstract Anemia is the most frequent complication of inflammatory bowel disease ( IBD ) , but anemia , mostly due to iron deficiency , has long been neglected in these patients .
The aim was to briefly present the pathophysiology , followed by a balanced overview of the different forms of iron replacement available , and subsequently , to perform a systematic review of studies performed in the last decade on the treatment of iron-deficiency anemia in IBD .