Transfusion haemosiderosis

Iron overload occurs in patients with transfusion dependent anaemia, notably thalassaemia major, Diamond-Blackfan syndrome, aplastic anaemia and acquired refractory anaemia. In many of these conditions iron overload is aggravated by physiological mechanisms which promote 130 increased dietary absorption of iron in response to ineffective erythro-poiesis. Each unit of blood contains 250mg iron and average transfusion dependent adult receives 6-10g of iron/year. Distribution of iron is similar to haemochromatosis with primarily liver parenchymal cell accumulation followed by pancreas, heart and other organs. Cardiac deposition occurs in patients who have received 100 units of blood (20g iron) without chelation, and is followed by damage to the liver, pancreas and endocrine glands.

Clinical features of iron overload in children who require transfusion support for hereditary anaemia are listed. Similar problems excluding those related to growth and sexual maturation develop in patients who commence a transfusion programme for acquired refractory anaemia in later life.

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