The possible use of desferrioxamine (DF) to measure body iron stores necessitated studies on the source of the iron excreted in the urine with the compound. DF did not take significant amounts of iron from transferrin because: (1) DF did not affect the plasma iron turnover (2) The excretion of a transferrin‐bound radioiron tracer was not increased by DF (3) Induced elevation of the plasma iron level was followed only by a slight increase in the iron excretion (4) No effect was observed on the incorporation into red cells of a transferrin‐bound radioiron tracer by DF Other studies indicated that iron, in the stage of being incorporated into red cell precursors, was not a probable source of the iron excreted with DF A significant delay in the excretion of iron with DF was regularly observed and found to be due to a delayed mobilisation of iron Further studies are necessary to find the source of iron excreted after administration of DF.

Because of the important role played by the liver in the synthesis of the plasma proteins, investigations of changes in the plasma protein pattern are used in the diagnosis of liver dysfunction. Some of the blood coagulation factors are proteins with specific activities which can be relatively easily and rapidly analyzed. Quantitative analyses of blood coagulation factors have therefore been utilized as liver function tests. The following clotting factors are more or less decreased in parenchymatous diseases of the liver: factor I (fibrinogen), factor I1 (prothrombin), factor V (proaccelerin), factor VII (proconvertin), factor IX (Christmas factor) and factor X (Stuart factor) (1,2,3,5,6,7,8,9,12,13,14,16,18,19,21,22). Factor VII, or factor V I I complex (factor V I I + factor X), has been found by most recent authors to diminish earlier and to a greater degree than the other clotting factors (1,2,5,6,8,12,23,33). The thromboplastin generation test, reflecting the combined activity of factors V, VIII, IX, and X

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The fraction of intravenously administered desferrioxamine (DF) and radioiron‐labelled ferrioxamine excreted with the urine varied within a narrow range in normal and iron‐deficient subjects. The DF‐induced urinary iron excretion is thus well correlated to the amount of iron chelated in the body. The variation in the amount of iron excreted with the urine after intravenous administration of 10 mg DF/kg body weight was studied in normal and iron‐deficient men and women. The iron excretion was significantly lower in iron‐deficient than in normal subjects, and it was lower in women than in men. The results showed that the iron excretion reflected the iron status of the body.

The desferrioxamine (DF)‐induced urinary iron excretion was measured in subjects in whom surgical biopsy specimens were used to determine liver non‐haemin iron. A very high correlation was observed between the increase of the urinary iron excretion after administration of DF on the one hand and the concentration of total non‐haemin, ferritin, and haemosiderin iron of the liver on the other. The studies were made in 10 female and 18 male subjects. Most subjects were considered normal with respect to liver function and iron state. Two male subjects with portal liver cirrhosis fell outside the normal relationship liver iron/urinary iron. The findings are discussed with special reference to the possible use of DF to quantitate iron stores.