Intravenous Iron Boosts Hemoglobin Levels in Children with Anemia, IBD

Paul A Rufo, MD

Credit: Boston Children's Hospital

In a single-center study, intravenous iron therapy proved safe and efficacious in improving hemoglobin levels in children and young adults with iron deficiency anemia (IDA) and active inflammatory bowel disease (IBD).¹

In contrast, results from the ​​longitudinal observational cohort study suggested oral iron or no iron therapy was generally ineffective for pediatric patients with IBD and active inflammation, demonstrating no significant changes in hemoglobin levels.

“Our data further demonstrate that addressing inflammation is insufficient to correct iron deficiency and that successful treatment of iron deficiency in pediatric patients without IBD warrants active management,” wrote the investigative team, led by Paul A Rufo, MD, an assistant professor at the Center for Inflammatory Bowel Disease at Boston Children's Hospital.

Anemia, commonly due to iron deficiency, is a frequent extraintestinal manifestation observed in IBD management.² Pediatric patients with IBD often exhibit IDA due to a variety of factors, including inadequate dietary intake, gastrointestinal blood loss, and reduced iron utilization. Persistent anemia can increase IBD-related mortality and patient quality of life inversely associated with its severity.

Evidence-based guidelines have recommended screening for IDA in the management of pediatric patients with IBD but may be limited in actual practice.³ Oral iron is a cost-effective method for IDA management but is also limited by poor compliance and decreased utilization. Intravenous iron therapy could be an effective approach to correct IDA—concerns about adverse reactions associated with its administration and the lack of published data on its clinical profile in children limit its utilization.⁴

Rufo and colleagues sought to assess the efficacy and safety of newer preparations of intravenous iron therapy for managing IDA in pediatric patients admitted to their tertiary care center for active IBD between September 2017 and December 2019.¹

IDA was diagnosed based on laboratory values and iron studies, including ferritin, serum iron, and total iron-binding capacity, collected on admission. Patients were then screened using electronic medical records to determine those with an established diagnosis of IBD, including ulcerative colitis (UC), Crohn’s disease (CD), and indeterminate colitis (IC).

The study design was uncontrolled, and clinicians treated patients with intravenous or oral iron supplementation, based on their clinical indication. As a result, some patients were discharged on no oral iron treatment at all. Efficacy of iron supplementation was marked as a ≥1 g/dL increase between pre- and post-treated hemoglobin levels and an improvement in iron status, based on iron studies.

Overall, 105 patients (44% of screened) met the criteria for IDA and 92 (40%) matched the study criteria. The population had an average age of 15 years and 41 (45%) were female. Among the cohort, 57 received intravenous iron, 17 received oral iron, and 18 were discharged before iron therapy.

Upon analysis, Rufo and colleagues identified a significant change in hemoglobin levels in those who received intravenous iron therapy (+1.9 mg/dL), compared with patients receiving oral (+0.8 mg/dL; P = .02) or no iron (0.8 g/dL; P = .03), respectively. The mean change in hemoglobin matched the study’s predetermined criteria for efficacy only in patients who received intravenous iron.

Safety data revealed only one out of 57 patients (1.8%; 95% CI, 0.04 - 0.09) who received intravenous iron experienced an adverse reaction, as indicated in their electronic medical record. The child was stabilized and required one additional day of inpatient observation before discharge.

Rufo and colleagues indicated IDA did not resolve in patients who had responded favorably to medical therapy, demonstrating comparable decreases in erythrocyte sedimentation rate and C-reactive protein levels. They noted the observation confirms the need for early identification and active management of IDA in a pediatric population with IBD.

“In contrast to previous tenets suggesting that iron deficiency would resolve when the underlying inflammation was corrected, our data suggest that in the absence of targeted iron therapy, correction of the underlying inflammatory response is insufficient to resolve iron homeostasis in patients with IBD,” Rufo and colleagues wrote.

References

1. _{Manokaran K, Spaan J, Cataldo G, et al. Inpatient management of iron deficiency anemia in pediatric patients with inflammatory bowel disease: A single center experience. World J Clin Pediatr. 2024;13(1):89318. Published 2024 Mar 9. doi:10.5409/wjcp.v13.i1.89318}
2. _{Rogler G, Vavricka S. Anemia in inflammatory bowel disease: an under-estimated problem?. Front Med (Lausanne). 2015;1:58. Published 2015 Jan 19. doi:10.3389/fmed.2014.00058}
3. _{Goyal A, Zheng Y, Albenberg LG, et al. Anemia in Children With Inflammatory Bowel Disease: A Position Paper by the IBD Committee of the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr. 2020;71(4):563-582. doi:10.1097/MPG.0000000000002885}
4. _{de Silva AD, Tsironi E, Feakins RM, Rampton DS. Efficacy and tolerability of oral iron therapy in inflammatory bowel disease: a prospective, comparative trial. Aliment Pharmacol Ther. 2005;22(11-12):1097-1105. doi:10.1111/j.1365-2036.2005.02700.x}