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Prepublished online as a Blood First Edition Paper on August 22, 2002; DOI 10.1182/blood-2002-06-1704.
Submitted June 11, 2002
Accepted August 5, 2002
Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias
Peter D Jensen*, Finn T Jensen, Thorkil Christensen, Johan L Nielsen, and Joergen Ellegaard
Department of Hematology, Aarhus University Hospital, Aarhus, Denmark
Center of Nuclear Magnetic Resonance, Aarhus University Hospital, Aarhus, Denmark
* Corresponding author; email: d222615{at}inet.uni2.dk.
The role of iron overload as cause of liver dysfunction has never been studied in detail in multiply transfused patients without concomitant hepatotropic infections. We therefore investigated the relationship between the extent of hepatocellular injury as reflected by serum levels of aminotransferase (ALT and AST) and several iron status indices in 39 adult anti-HCV-negative non-thalassemic patients with transfusional iron overload owing to acquired anemias. In 12 patients, we monitored aminotransferase levels and indices of iron status during iron chelation treatment. Before treatment, elevated aminotransferase activity was only seen at liver iron concentrations >300 µmol/g. During treatment all aminotransferase values were normal if the liver iron concentration returned below 350 µmol/g. At start of treatment, ALT (R2=0.64, P= .006) and AST activity (R2= 0.57, P= .01) were closely related to urinary iron excretion, reflecting the size of the chelatable or the labile iron pool. During treatment, a comparable pattern was seen and the urinary iron excretion was also directly related to the liver iron concentration at concentrations above approximately 400 µmol/g. All elevated ALT values were associated with a urinary iron excretion >15 mg/24 h. In conclusion, our data suggest the existence of a critical liver iron concentration range, above which hepatocellular injury is seen. The extent of the injury seems to be determined mainly by the size of the chelatable or labile iron pool, supporting the concept of the labile iron pool as the compartment directly involved in iron toxicity. Our findings may be helpful in establishing criteria for safety from complications of transfusional iron overload.
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