Transfusion-associated iron overload

Research output: Contribution to journalShort survey

18 Citations (Scopus)

Abstract

Iron overload develops mainly via two mechanisms, by a defect in the regulation of iron absorption (hereditary hemochromatosis) or by parenteral route (chronic red cell transfusion for anemic patients without blood loss) 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 (hepatic magnetic susceptibility, CT, and magnetic resonance imaging) 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 HLA-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.

Original languageEnglish
Pages (from-to)436-441
Number of pages6
JournalCurrent Opinion in Hematology
Volume4
Issue number6
DOIs
Publication statusPublished - Jan 1 1997

ASJC Scopus subject areas

  • Hematology

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