Zinc-associated Copper Deficiency Myelopathy: A Case Report.

OBJECTIVE

Copper deficiency myelopathy is an uncommon but potentially reversible neurologic disorder characterized by sensory ataxia, gait impairment, and dorsal column dysfunction. Acquired copper deficiency most commonly results from malabsorption, prior gastrointestinal surgery, or excess zinc exposure. Zinc induces intestinal metallothionein, which preferentially binds copper and reduces its systemic absorption, potentially leading to hypocupremia and neurologic dysfunction. Although zinc-containing nutritional supplements are widely used, clinically significant neurologic complications remain rare.

METHODS

A retrospective review of the patient's medical history was performed in addition to a comprehensive literature review.

RESULTS

A 70-year-old woman receiving long-term zinc-containing PreserVision AREDS 2 supplementation for age-related macular degeneration presented with 6 months of progressive paresthesia, gait instability, and frequent falls. Neurologic examination demonstrated bilateral sensory deficits and weakness, while magnetic resonance imaging revealed dorsal column T2 hyperintensity. Laboratory evaluation showed undetectable serum copper, mildly elevated serum zinc, normocytic anemia, hypokalemia, and concurrent thiamine deficiency. Zinc-containing supplementation was discontinued, and the patient received copper and thiamine replacement. Over the following two months, serum copper normalized, and she experienced substantial neurologic recovery with restoration of independent ambulation.

CONCLUSIONS

This report describes a case of copper deficiency myelopathy in a patient receiving long-term high-dose zinc supplementation in the setting of multiple nutritional abnormalities. It highlights the importance of including copper deficiency in the differential diagnosis of patients receiving zinc-containing supplements who present with progressive myelopathy. It is intended to be hypothesis-generating and suggests that individual susceptibility and concurrent nutritional factors may contribute to the development of zinc-associated copper deficiency.