A Hematologic Twist: Zinc-Induced Copper Deficiency Mimicking Myelodysplastic Syndrome

Abstract

Zinc-induced copper deficiency is an underdiagnosed condition that can lead to systemic manifestations of hypocupremia, including anemia, neutropenia, ataxic myelopathy, spastic paresis, alopecia, and skin depigmentation. This case illustrates the harmful effects of zinc supplementation and zinc-containing denture adhesive in a 68-year-old man, ultimately leading to copper deficiency. It also underscores the importance of considering zinc toxicity in the differential diagnosis of patients presenting with unexplained cytopenias, bone marrow abnormalities, and related symptoms. Furthermore, this report highlights the need for clinicians to consider zinc toxicity-induced copper deficiency in the evaluation of unexplained pancytopenias, especially in the post-COVID era, where zinc supplementation has become increasingly prevalent.

Keywords: denture adhesives; myelodysplastic syndromes; supplement risks; unexplained anemia; unexplained neutropenia; zinc excess; zinc-induced hypocupremia.

Figure 1. Mechanism of zinc-induced copper deficiency.

This diagram illustrates how excess zinc disrupts copper absorption in the small intestine. In the jejunal enterocyte, elevated zinc levels stimulate increased production of metallothionein, a metal-binding protein. Metallothionein has a higher affinity for copper than for zinc, leading to preferential binding of copper ions. As enterocytes undergo natural turnover and are sloughed off, the copper bound to metallothionein is lost in the feces. This process reduces systemic copper absorption, ultimately resulting in hypocupremia. This mechanism explains the hematologic and neurologic manifestations observed in zinc-induced copper deficiency. This image was created using DALL·E, an AI-based illustration tool [15].