Copper deficiency anaemia

Abstract

A 27-year-old man with myoclonic epilepsy, who had been receiving enteral nutrition through a nasogastric tube for 6 years, was found to have microcytic, hypochromic anaemia and neutropenia. Haematological data included red cell count 2·42 × 1012/l, haematocrit 0·2 l/l, haemoglobin 6·5 g/dl (MCV 81·8 fl, MCH 26·0 pg, MCHC 31·8 g/dl), white cell count 2·3 × 109/l (neutrophil count 0·5 × 109/l, lymphocyte count 1·3 × 109/l, monocyte count 0·5 × 109/l), and platelet count 118 × 109/l. A bone marrow aspirate showed maturation arrest of the myeloid series, cytoplasmic vacuoles in the immature erythroid and myeloid cells (left, Wright's stain), and 29% ringed sideroblasts (right, Prussian blue stain). The serum iron, unsaturated iron binding capacity, and ferritin were all within normal limits. The serum copper was 0·47 μmol/l (normal, 12·25–20·57 μmol/l) and ceruloplasmin 8 mg/dl (normal, 18–37 mg/dl). Thus, the patient was diagnosed with copper deficiency anaemia. He was taking the commercially prepared formula, containing 0·144 mg of copper daily, which was far below the recommended daily dosage of 2–3 mg copper; the formula was therefore supplemented with copper sulphate (2·6 mg elemental copper) daily. The haematological and bone marrow abnormalities were corrected in 1 month. Ceruloplasmin and copper enzymes such as cytochrome oxidase and superoxide dismutase are required for iron transport, haem synthesis, and optimal erythrocyte membrane function, respectively. Patients receiving long-term enteral or parenteral alimentation with copper-free/deficient solutions should be given copper supplementation.