Contents
Copper deficiency is a disease that causes cytopaenia and neuropathy and can be treated by copper supplementation.
Physiology
Adequate copper intake permits normal utilization of dietary iron in that intestinal iron absorption, iron release from stores (e.g. in macrophages of liver and spleen), and iron incorporation into hemoglobin are copper-dependent processes. In addition to preventing anemia, copper assists in blood coagulation and blood pressure control; cross-linking of connective tissues in arteries, bones, and heart; defense against oxidative damage; energy transformation; myelination of brain and spinal cord; reproduction; and synthesis of hormones.
Copper metabolism:
Aetiology
Risk factors:
- Special nutritional conditions: Long-term tube feeding, long-term total parenteral nutrition (TPN)
- Intestinal resection
- Ingestion of zinc
Clinical features
Hematological presentation:
- Anemia (microcytic, normocytic, or macrocytic)
- Neutropenia
- Thrombocytopenia (rare)
Neurological manifestations:
- Myelopathy
- Peripheral neuropathy (simulating subacute combined degeneration)
Bone marrow findings:
Mimic myelodysplasia resulting in occasional inappropriate referral for bone marrow transplantation
Case study:
Diagnosis
Hematological, but not neurological, manifestations respond promptly to copper replacement, making early diagnosis essential for good outcome.
Differential diagnosis:
Other conditions with similar presentations
- Infections, drug toxicity, autoimmunity, B12 deficiency, folate deficiency, myelodysplastic syndrome, aplastic anemia, and lymphoma with bone marrow involvement
Management
Neurological symptoms will become irreversible if treatment is delayed making it crucial to diagnose copper deficiency and start treatment early.
Copper supplementation