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Copper deficiency, or hypocupremia, is an uncommon but clinically significant nutritional disorder affecting hematologic and neurologic systems. While inherited forms like Menkes syndrome occur in infants, acquired deficiency is more common in adults. Primary causes include excessive zinc intake (which blocks copper absorption), malabsorption disorders (celiac disease, Crohn's disease, cystic fibrosis), and weight-loss or bariatric surgery.

Clinical manifestations are nonspecific but severe. Hematologic effects include hypochromic anemia unresponsive to iron and neutropenia (low white blood cells), increasing infection risk. Neurologic complications involve myeloneuropathy mimicking vitamin B12 deficiency, with symptoms like tingling, numbness, gait abnormalities, and loss of sensation in hands and feet. Other signs include fatigue, muscle weakness, osteoporosis, skin hypopigmentation, and "steely" or kinky hair.

Copper is essential for blood cell formation, collagen synthesis, melanin production, immune function, and nerve communication. Healthy individuals require 0.9 mg/day orally. Diagnosis involves measuring serum copper and ceruloplasmin levels. Treatment requires addressing the underlying cause and intravenous copper repletion, often at 4–8 times the usual nutritional doses for severe cases.