Abstract Background Alterations of iron metabolism in Crohn's disease (CD) adversely affect patients’ quality of life, with anaemia being a main clinical manifestation. The causes of anaemia in CD are multifaceted. Our goal is to outline the initial iron metabolism features in a treatment-naïve CD cohort, offering clinical insights to enhance therapeutic approaches. Methods We enrolled CD patients from a prospective inception cohort between July 2019 and June 2022 undergoing treatment with tumour necrosis factor antagonists and collected results of blood routine tests, C-reactive protein, iron metabolism markers, and plasma samples at the time of diagnosis. Follow-up for 70 patients was conducted 3-6 months post-treatment, with hepcidin levels measured using enzyme-linked immunosorbent assay kits. Results In our baseline analysis of 141 CD patients, 106 were male (75.2%) with a median diagnostic age of 25 (Table). Anaemia was present in 73 patients (51.8%), with 9 having moderate anaemia (12.3%). Three patients received oral iron during follow-up. Patients were categorized into three ferritin-based groups: 33 in Group 1 (ferritin <30, 23.4%), 58 in Group 2 (ferritin 30-100, 41.1%), and 50 in Group 3 (ferritin >100, 35.5%). Group 1 had the fewest male patients (54.4% vs. 81%/82%, P < 0.017), while Group 3 had the highest C-reactive protein and the lowest albumin levels. Group 1 had lower white blood cell (6.5 vs. 7.8, P = 0.007), neutrophil counts (4.5 vs. 5.4, P = 0.01), and less colorectal involvement (45.4% vs. 78.0%, P = 0.004) than Group 3. Group 1 had a higher proportion of anaemia (66.7% vs. 39.7%, P = 0.013), and lower values in red blood cell morphology parameters compared to Group 2. Ferritin correlated strongly with hepcidin (r=0.835, P < 0.001), and transferrin moderately (r=-0.571, P < 0.001). In the follow-up of 70 patients (Figure A), anaemia state and abnormal Mean corpuscular volume significantly improved after biological therapy (51.4% vs. 14.3% and 65.7% vs. 32.9%, respectively), while the proportion of patients in Group 1 increased significantly (21.4% vs. 42.9%). Further analysis of iron metabolism indicators before and after treatment (Figure B) revealed significant decreases in hepcidin and ferritin, and a significant increase in transferrin across all three ferritin-based groups. Conclusion Iron metabolism disruptions and insufficient iron reserves contribute to anaemia in CD, which correlates with sex, disease location, and the severity of inflammation. After biological therapy, anaemia significantly improved, but iron reserve indicators decreased. The anaemia improvement seems due to reduced inflammation rather than iron supplementation, highlighting the need to monitor iron reserves to refine anaemia management in CD.
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