Iron Deficiency Anemia in Inflammatory Bowel Diseases-A Narrative Review

Abstract

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is characterized by chronic inflammation of the gastrointestinal tract. IBD has been associated with numerous symptoms and complications, with the most common being iron deficiency anemia (IDA). Iron deficiency in IBD is caused by inadequate intake, malabsorption (including duodenal involvement and surgical removal), and chronic blood loss by mucosal ulcerations. Therefore, an appropriate diet should be enforced. Iron deficiency and iron supplementation have been associated with alterations to gut microbiota. IBD-associated anemia, in particular iron deficiency anemia, is associated with a significant decrease in quality of life and with clinical symptoms such as chronic fatigue, headaches and dizziness, reduced exercise tolerance, pale skin, nails, conjunctiva, and fainting. However, despite these numerous adverse symptoms, IDA remains undertreated. The European Crohn's and Colitis Organisation (ECCO) guidelines state that patients should be monitored for anemia. Adequate treatment, whether oral or intravenous, should be implemented while taking into consideration C-reactive protein values (CRP), hemoglobin levels, and therapeutic response. It should be stressed that every case of anemia in IBD patients should be treated. Intravenous iron formulations, which are more superior compared to the oral form, should be used. There is a need to increase awareness and implementation of international guidelines on iron supplementation in patients with IBD.

Keywords: IBD; IDA; dietary factors; dysbiosis; iron deficiency; iron metabolism; microbiota.

Figure 1

The effect of inflammation in IBD (inflammatory bowel disease) is mainly mediated by hepcidin [24]. Hepcidin is a peptide hormone produced in the liver. It plays a key role in regulating iron homeostasis. It is a direct inhibitor of ferroportin—a protein that transports iron beyond the cells that store it. The hepcidin–FPN (ferroportin) axis is considered to be the main regulator of iron homeostasis [24]. Inhibited ferroportin, present on enterocytes and macrophages, inhibits the transport of iron from enterocytes to the hepatic portal vein system, thus reducing iron absorption. Inhibited ferroportin leads to an inhibition of iron export, which is mainly found in the intestinal epithelium, macrophages, and hepatocytes. Consequently, the transport of iron absorbed by the intestines into the circulation and the release of iron from other cells is inhibited, which results in lowering the iron content in the serum. The inflammatory reaction significantly affects iron metabolism in the human body. The role of hepcidin explains the relationship between the immune response and iron metabolism [25,26].

Figure 2

The advantages and drawbacks of oral supplements.