Copper deficiency can lead to anemia, leukopenia, or thrombocytopenia, often mimicking vitamin B12 deficiency or myelodysplastic syndrome. We review the crucial role of copper in iron metabolism and hematopoiesis, highlighting how high-dose zinc supplementation, gastrointestinal surgeries, and long-term nutritional support can induce deficiency. The pathophysiology involves compromised ferroxidase activity, which hampers iron utilization, and reduced neutrophil survival due to impairment of cytochrome c oxidase and superoxide dismutase. Timely recognition is vital, as most cases respond to copper repletion and zinc reduction. Institutional data underscore the need for routine copper monitoring, and management strategies aim to optimize patient care by maintaining adequate copper levels.
Keywords: Anemia; Ceruloplasmin; Copper deficiency; Enteral nutrition; Zinc.
© 2025. The Author(s), under exclusive licence to Japanese Society of Hematology.