Patients who are chronically dependent on red cell transfusions (e.g. thalassaemia, sickle cell disease, myelodysplastic syndrome and red cell aplasia) are at the biggest risk of iron overload. The body cannot remove excess iron which accumulates over time in certain organs such as the liver, heart and endocrine organs affecting their function.
Early symptoms are often vague such as muscle weakness, fatigue and weight loss. Later, skin pigmentation, arthropathy, diabetes, impotence, cardiac failure and hepatic dysfunction can occur.
Liver disease is the most common complication of transfusion iron overload and iron cardiomyopathy is the leading cause of death in patients with thalassaemia.
Each unit of red cells contains about 250 mg of iron and the average rate of iron excretion is only about 1 mg/day. As a cumulative effect of regular transfusions, iron overload can occur and should be suspected after transfusion of as few as 10 red cell units. Major morbidity and mortality may be associated with cumulative doses of 20 or more units.
The severity of iron overload can be determined by:
Treatment is aimed at the removal of accumulated iron in the tissues e.g. using iron-chelating agents which form complexes with iron and promote its excretion.
Updated June 2025