Transfusion iron overload in adults with acute leukemia: manifestations and therapy.

Abstract

Hepatic dysfunction occurs commonly among persons successfully treated for acute leukemia, and iron overload is a possible cause of hepatic and other abnormalities in these patients. We identified 5 adults 40+/-13 (mean +/- S.D.) years of age who developed transfusion iron overload in association with successful chemotherapy of de novo acute leukemia. None had evidence of hemochromatosis, viral hepatitis, or other primary hepatic disorders. The mean serum ferritin concentration of our patients was 1531+/-572 ng/mL. Other abnormalities associated with transfusion iron overload were increased stainable iron in bone marrow macrophages, elevated serum concentrations of hepatic enzymes, hyperpigmentation, hyperferremia, elevated iron saturation of serum transferrin, and increased stainable iron in Kupffer cells and hepatocytes. Rheumatologic, endocrinologic, or cardiac abnormalities attributable to iron overload were not observed. Therapeutic phlebotomy was initiated after chemotherapy; recovery of hemoglobin concentrations after phlebotomy permitted weekly treatment in each case. This yielded an average of 28+/-9 units per patient (range 15-35 units). Abnormalities associated with transfusion iron overload resolved after iron depletion therapy. The mean leukemia-free survival of our patients is 96+/-36 months (range 40-125 months). Our data and those of others suggest that 15 to 20% of adults who are long-term survivors of acute leukemia develop iron overload, often with hepatic abnormalities. Iron overload is a relatively common sequela to successful management of acute leukemia in adults for which routine evaluation should be performed and for which therapeutic phlebotomy should be used as treatment.