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Prepublished online as a Blood First Edition Paper on August 22, 2002; DOI 10.1182/blood-2002-06-1704.
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Blood, 1 January 2003, Vol. 101, No. 1, pp. 91-96
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
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
From the Department of Hematology and Center for
Nuclear Magnetic Resonance, Aarhus University Hospital, Aarhus,
Denmark.
The role of iron overload as cause of liver dysfunction has never
been studied in detail in patients without concomitant hepatotropic infections who receive multiple transfusions. We therefore investigated the relationship between the extent of hepatocellular injury as reflected by serum levels of aminotransferases (alanine
aminotransferase [ALT] and aspartate aminotransferase [AST]) and
several iron status indices in 39 anti-hepatitis C virus-negative
(HCV ) nonthalassemic 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 seen only at liver iron concentrations more than 300 µM/g. During treatment all aminotransferase values were
normal if the liver iron concentration returned below 350 µM/g. At
the 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 µM/g. All elevated ALT values
were associated with a urinary iron excretion more than 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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