Figure 3.

Mechanisms of iron deficiency anemia in celiac disease.In normal conditions, iron is absorbed in the gastrointestinal tract and then delivered to transferrin for transport to developing red cells; excess iron is stored in hepatocytes. In celiac disease, due to the atrophy of the intestinal mucosa, there is a reduced intestinal absorption of iron and therefore reduced iron delivery to developing red cells. Furthermore, the concomitant inflammation of the mucosa induced by gluten causes the increased release of cytokines, which can induce increased hepatic hepcidin production; hepcidin inhibits ferroportin, the main iron-export protein, and it consequently reduces iron release from enterocytes, hepatocytes, and circulating macrophages. DMT1: divalent metal transporter 1; DCYTB: duodenal cytochrome B. Adapted from DeLoughery et al. [55].