Iron overload develops mainly via two mechanisms, by a defect in the regulation of iron absorption lpar;hereditary hemochromatosisrpar; or by parenteral route lpar;chronic red cell transfusion for anemic patients without blood lossrpar; especially in patients with different categories of refractory anemias, and in anemic patients with chronic infection, alcohol excess, and malignancies. The accurate assessment of body iron is indispensable for the correct diagnosis and for finding the optimal treatment schedule for each individual patient. Liver biopsy with quantitative iron determination and histochemistry is still the reference method for the assessment of body iron status for patients with iron overload. New noninvasive measurements lpar;hepatic magnetic susceptibility, CT, and magnetic resonance imagingrpar; are still investigational procedures. It is important to decrease the need for transfusion by judicious use of red cell concentrates, make more widespread use of erythrocytapheresis, determine the red blood cell phenotype of the patient before the onset of a regular transfusion regimen, treat concomitant hepatitis infections, consider splenectomy to diminish red blood cell requirements, and early on consider allogeneic bone marrow transplantation for thalassemic patients who have HLAhyphen;identical siblings. It is advisable to screen for the hereditary hemochromatosis gene before starting any kind of regular red blood cell transfusion therapy, and to avoid if possible, the risk of free radical release by transfusional iron overload during the physiologically hypercoagulable state of pregnancy and its effects on the highly proliferative tissues of the fetus.
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