[Posttransfusion iron overload]

Patients receiving red cell concentration regularly are liable to develop iron overload. The characteristic feature of this condition is higher than normal generalized iron depositing. Iron excess initially is deposited in the liver, reticuloendothelial system, and consequently in such organs as the heart and endocrine glands. Humans do not possess mechanisms to excrete the excess of this metal. Patients who have undergone long time hemotherapy develop manifestations of diabetes, liver cirrhosis or cardiomyopathy; the most common cause of death is heart failure. Posttransfusion iron overload is observed most often in patients with thalassemia, aplastic and hemolytic syndromes and with syderoplastic anemias. An interesting fact is that numerous and long time transfusions in patients with chronic bleeding do not results in iron overload. Each transfused unit of red cell concentrate delivers approximately 250 mg of iron, thus iron accumulation is an inevitable effect of long time red cell concentrate therapy. Excessive iron intake manifests clinically when the total iron level reaches 400-1000 mg/kg b.m. The clinical picture resulting from posttransfusion iron overload includes dark skin, liver cirrhosis and circulatory disorders in the form of arrhythmia and insufficiency (of left ventricle, particularly). Iron overload can be treated but it is better to prevent it by administering chelating drugs. These compounds have high affinity and specificity to iron. They eliminate it with urine in the form of a bound complex. The use of chelating drugs is recommended when around 20 red cell concentrate units have been transfused and the serum ferritin level is about 1000 microg/ml.