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Myeloneuropathy and anemia due to copper malabsorption
1Department of Neurology, E8A Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA. kumar.neeraj@mayo.edu
Journal of Neurology
|August 18, 2004
Summary
Copper malabsorption can cause neurological issues in adults, mimicking vitamin B12 deficiency. Supplementation halted neurological decline in a 63-year-old woman with acquired copper deficiency.
Area of Science:
- Neurology
- Nutritional Science
- Biochemistry
Background:
- Copper is essential for neurological function, and its deficiency causes swayback in ruminants.
- Menkes disease, a genetic disorder of copper absorption, typically results in early mortality.
- Acquired copper deficiency in humans is rare, especially presenting with myeloneuropathy in adulthood.
Observation:
- A 63-year-old woman presented with progressive myeloneuropathy.
- The patient had a history of copper malabsorption.
- Neurological symptoms included ataxia and myelopathy.
Findings:
- Copper supplementation effectively halted the neurological deterioration in the patient.
- The clinical presentation of acquired copper deficiency myeloneuropathy resembled that of vitamin B12 deficiency.
- This case highlights the potential for adult-onset neurological disease due to copper malabsorption.
Implications:
- Adults can develop severe neurological complications from acquired copper deficiency.
- Copper malabsorption should be considered in the differential diagnosis of myeloneuropathy, particularly when vitamin B12 deficiency is ruled out.
- Timely copper supplementation may reverse or halt neurological damage in acquired copper deficiency states.