Abstract
Anemia is one of the most frequent complications and/or extraintestinal manifestations of inflammatory bowel disease (IBD). Iron deficiency is the most important cause of anemia in Crohn’s disease and ulcerative colitis patients. Iron deficiency even without anemia may impact the quality of life of our IBD patients. In the last 10 years, the understanding of the pathology of iron-deficiency anemia and “anemia of chronic diseases” has increased; new diagnostic tools have been developed and new therapeutic strategies have been discussed. Hepcidin has been identified to be a central regulator of iron absorption from the intestine and of iron plasma levels. Hepcidin is regulated by iron deficiency but also as an acute phase protein by pro-inflammatory mediators such as interleukin-6. Innovative diagnostic tools have not been introduced in clinical routine or are not available for routine diagnostics. As iron substitution therapy is easy these days with a preference for intravenous substitution, the impact of differential diagnosis of anemia in IBD patients is underestimated.
Highlights
When we looked into patient data of a cross-sectional cohort in Switzerland, we found anemia in 12.9% of inflammatory bowel disease (IBD) patients in private practice, and 28.8% of www.frontiersin.org
Hepcidin induced by pro-inflammatory mediators such as IL-6 in IBD patients may contribute to the lower efficacy of oral iron substitution therapy in IBD patients [86, 87] leading to ACD
SUMMARY New insights in the pathophysiology of iron deficiency and anemia have been obtained in recent years
Summary
Iron deficiency is the most important cause of anemia in Crohn’s disease and ulcerative colitis patients. Iron deficiency even without anemia may impact the quality of life of our IBD patients. On the other hand during anemia of chronic diseases (without significant iron deficiency), hepcidin expression is even increased, which may explain why iron is “trapped” intracellularly under these conditions [46] (Figure 2A).
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