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<p>Copper deficiency is a rare yet reversible cause of anemia and bone marrow dysplasia that can mimic myelodysplastic syndrome (MDS), especially in patients on maintenance dialysis, who are at increased risk due to trace element losses, chronic inflammation, and impaired absorption. We report a 69-year-old woman on long-term hemodialysis with a history of partial gastrectomy who developed macrocytic anemia refractory to erythropoiesis-stimulating agents (ESAs). Bone marrow examination revealed erythroid dysplasia, hypocellularity, and ring sideroblasts. Although serum copper levels were initially within the low-normal range, the clinical course was consistent with functional copper deficiency, which progressed to absolute deficiency following brief zinc supplementation. Oral copper therapy was ineffective, whereas intravenous copper sulfate led to rapid hematologic recovery and resolution of dysplastic changes on follow-up biopsy. This case highlights the diagnostic complexity of ESA-resistant anemia in dialysis patients with overlapping risk factors and underscores the need to consider functional micronutrient deficiencies even when serum levels appear normal.</p>

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Diagnostic pitfalls of ESA-resistant anemia due to functional copper deficiency in a dialysis patient: a myelodysplastic syndrome mimic

  • 期刊论文

  • 发表日期：

    2026年1月27日

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  • Yukinobu Ikegishi,
  • Rokuo Abe,
  • Akiko Maehata,
  • Yoshihisa Takiyama

摘要

Copper deficiency is a rare yet reversible cause of anemia and bone marrow dysplasia that can mimic myelodysplastic syndrome (MDS), especially in patients on maintenance dialysis, who are at increased risk due to trace element losses, chronic inflammation, and impaired absorption. We report a 69-year-old woman on long-term hemodialysis with a history of partial gastrectomy who developed macrocytic anemia refractory to erythropoiesis-stimulating agents (ESAs). Bone marrow examination revealed erythroid dysplasia, hypocellularity, and ring sideroblasts. Although serum copper levels were initially within the low-normal range, the clinical course was consistent with functional copper deficiency, which progressed to absolute deficiency following brief zinc supplementation. Oral copper therapy was ineffective, whereas intravenous copper sulfate led to rapid hematologic recovery and resolution of dysplastic changes on follow-up biopsy. This case highlights the diagnostic complexity of ESA-resistant anemia in dialysis patients with overlapping risk factors and underscores the need to consider functional micronutrient deficiencies even when serum levels appear normal.