SUMMARY The chelation of body iron by desferrioxamine methanesulphonate in patients with haemolytic anaemias of varying types, in megaloblastic and in sideroblastic anaemias was measured by the differential ferrioxamine test. Thirty‐five out of 44 patients studied had chelation values above the normal range, sometimes exceeding those found in untreated haemochromatosis. In the haemolytic anaemias, the amount of chelation increased with the severity of the anaemia. In the megaloblastic anaemias, specific therapy reduced the amount of iron chelated by desferrioxamine at the same time as normal erythropoiesis was re‐established. Concepts of labile iron and metabolically active iron are compared with desferrioxamine chelatable iron. These findings suggest that in addition to storage iron (ferritin‐haemosiderin) chelated with difficulty, there is a compartment of readily chelatable iron derived from haem catabolism, possibly sited in reticulo‐endothelium. A model of intracellular iron transport in reticulo‐endothelial cells is proposed which provides a primary pathway of metabolically active, highly chelatable iron derived from haemoglobin catabolism, and a secondary pathway to intracellular ferritin.

Nine children with acute promyelocytic leukemia (APL) are presented. This series of children represents 7% of all acute leukemias and 21% of acute myelogenous leukemias seen during the same period at the Red Cross War Memorial Children's Hospital. These figures are much higher than the incidence quoted in other series of childhood leukemia. In addition, most of those children came from a confined geographic area. Two of the patients were younger than 2 years of age. The youngest patient with APL previously reported in the literature was 24 months.

SUMMARY We present the findings of a survey to determine the prevalence of inherited haemoglobin disorders in the Coloured (mixed ethnic origin) population of South Africa. A variety of haemoglobins was found. Of the structural variants, Hb E and Hb S were the most common, the former probably originating from South-East Asia and the latter from East Africa and possibly Madagascar. The oa+ (-cx) for Hb E (Hb AE) and Hb C (Hb AC) were estimated at 0-9% and 0-3% respectively for the Cape Malay Coloured population and as 1% and 0.3% for the non-Malay Coloured group.2 In the white population, the same survey gave the following frequency estimation: Hb AS 0-2%, Hb AE 0-2%, and Hb AC 0-4%, but these figures seem rather high for a purely Caucasian population. Reports of homozygous Hb C disease in a white family have been published,6 7 but a report of sickle cell anaemia in this population group is difficult to substantiate.8 The rarity of the sickle cell gene among South African Blacks is well documented.9 "' Haemoglobin S has been described in a South African Indian population," including reports of the homozygous state,'2 13 but we are

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