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P083. Divalent metal-ion transporter 1 deficiency contributes to the anemia in inflammatory bowel disease

C. Liu, W. Wu, T. Chen, L. Fang, M. Sun, R. Wu, Z. Liu, Shanghai Tenth People's Hospital, Tongji University, Department of Gastroenterology, Shanghai, China


Patients with inflammatory bowel disease (IBD) often have anemia which is recognized as a complication. Divalent metal-ion transporter 1 (DMT1) and ferroportin 1 (Fpn1) have been reported to play important roles in the hemogenesis. In this study, we aimed to investigate the potential role of DMT1 and Fpn1 in the pathogenesis of anemia.


We performed a retrospective study including 71 patients with Crohn's disease (CD), 31 patients with ulcerative colitis (UC), and 30 healthy age-matched healthy donors. Hemoglobin (Hb), serum iron, ferritin, transferrin, transferrin receptor, total iron binding capacity, folic acid, vitamin B12, erythropoietin (Epo) and C-reactive protein (CRP) were detected, and expressions of DMT1 and Fpn1 in inflamed mucosa of IBD patients or normal controls were determined by quantitative real-time polymerase chain reaction and immunohistochemistry.


In 102 patients with IBD, 87.71% of patients in CD and 68.70% in UC had anemia. The levels of serum iron in IBD patients with anemia were significantly lower than controls (P < 0.05). Serum iron showed a significant correlation with levels of Hb in both CD and UC patients (P < 0.05). However, the concentrations of folate and vitamin B12 were not related with Hb in this kind of anemia. Furthermore, DMT1 was found to be significantly decreased in the inflamed mucosa of IBD patients, but Fpn1 expression was markedly increased in intestinal tissues compared with normal controls (P < 0.05).


Anemia is commonly seen in IBD patients and mainly caused by lack of serum iron. Decreased expression of DMT1 in intestinal mucosa leads to compromised transfer of iron into intestinal epithelial cells. Thus, this work provides a therapeutic approach in the management of anemia in IBD.