MECHANISM OF DESFERRIOXAMINE-INDUCED IRON EXCRETION IN THALASSEMIA

The mechanism of desferrioxamine (DF)‐induced iron excretion was investigated in 16 thalassaemic patients. Transferrin‐59Fe has been injected intravenously and the fraction of radioiron located to iron stores was determined as the difference between total injected 59Fe and % RBC utilization. Following the intravenous infusion of 4 g DF, the specific acitivity of excreted urinary iron has been measured in 11 patients and the total chelatable pool was calculated as (100–% RBC utilization)/specific activity of urinary iron. Despite the wide variation in DF induced urinary iron excretion, ranging from 3 to 86 mg/d, an unexpected uniformity in the specific activity of chelated urinary iron was found in all patients, and the calculated chelatable pool was 4.5±1.2 (mean±SD) g of iron. These findings suggested that iron chelated by DF was probably not obtained directly from the total storage iron pool but rather from a smaller high specific activity iron compartment derived from the catabolism of labelled non‐viable erythrocytes. This postulate was tested by the direct measurement of specific activities in the liver and spleen in five patients undergoing surgery. In all patients, the specific activity of splenic non‐haem iron representing RE iron stores (31±8%59Fe/gFe), was much higher than that of hepatic iron (2±1%), and the specific activity of iron excreted in the urine (30p8%) was identical with the specific activity of splenic iron. These findings indicate that DF‐induced urinary iron excretion is derived from a chelatable pool located in the RE system. Copyright © 1979, Wiley Blackwell. All rights reserved