Although the anaemia associated with chronic disorders is one of the most frequently encountered forms of anaemia, particularly in hospital patients, it has not received the distinction which it deserves, in part, perhaps, because of the lack of an appropriate name. The term ‘simple chronic anaemia’ is most inappropriate because the pathogenesis of the anaemia involves the delicate control mechanisms of erythropoiesis and these are not simple. The title ‘anaemia of chronic infections’ is much too restrictive, for the anaemia occurs in patients with cancer, lymphoma, rheumatoid arthritis, collagen vascular diseases, fractures, severe tissue injury and many other disorders. ‘Anaemia of chronic disorders’, though a less restrictive title, is unsatisfactory because many other types of anaemia occur in these disorders, such as blood loss, overt haemolytic anaemia of various types, reactions to drugs, myelophthisic anaemia, and the anaemia of renal failure. Furthermore, the name gives no hint as to the diagnostic features or pathogenesis of the anaemia. A more descriptive, but somewhat more cumbersome, title might be ‘sideropenic anaemia with reticuloendothelial siderosis.’

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1. Two morphologically distinct populations of erythrocytes were found in a mother and in two of her daughters, one of whom (the proband) was anemic. One erythrocyte population was morphologically normal; the other was hypochromic and microcytic. 2. The X-linked blood group antigen, Xga, was present in erythrocytes from the mother and the two daughters, but not in erythrocytes from the father. The daughters were, therefore, heterozygous for the gene controlling this antigen. 3. Separation of the two populations of erythrocytes was accomplished by centrifugation in layered gum acacia solutions of different specific gravity. 4. The microcytic cells from the three affected individuals were Xga-positive. Isolated normal cells were Xga-positive in the mother, but negative in both daughters. These data suggest that the erythrocyte defect is X-linked and that the phenomenon of X-inactivation applies to genes controlling both the morphologic defect and the Xga antigen. 5. The free protoporphyrin content of the isolated microcytes was lower than that of the normal cells. The capacity of the microcytes to convert delta-aminolevulinic acid to protoporphyrin was unimpaired. On these bases it is suggested that the hereditary defect lies either at or before the step in which delta-aminolevulinic acid is synthesized.

In a 10-yr observation period, 75 patients with multiple myeloma have been studied, and 55 of these were treated daily with low dose melphalan by mouth. Of these, four developed sideroblastic anemia, manifested by anemia, thrombocytopenia, aniso-poikilocytosis, and hypochromic stippled cells in the blood, and ringed sideroblasts in the bone marrow. In two patients, this complication occurred after more than 7 yr of therapy and at a time when there was no evidence of myeloma. In a third patient, it occurred when the myeloma relapsed, and in the fourth, myeloma was active but stable. The anemia did not respond to either folate or pyridoxine. In all four patients, acute myelomonoblastic leukemia developed within 6 mo after sideroblastic anemia had been detected. These observations suggest that sideroblastic anemia in myeloma is a preleukemic manifestation.

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