Similarities of the erythrocytes in juvenile chronic myelogenous leukemia to fetal erythrocytes.

A 4-yr-old boy was studied who placed to the left of the curve from showed typical findings of juvenile normal adult blood; the hemoglobin chronic myelogenous leukemia, inA2 level and the erythrocyte I antigen cluding massive hepatosplenomegaly, titer were reduced; and a structural thrombocytopenia, low leukocyte alkaanalysis of the ‘i-chain of the fetal line phosphatase, and absence of a hemoglobin showed the glycine to alaPhiladelphia chromosome. The erythnine ratio in ‘v-136 to be typical of the rocytes of the patient exhibited many neonatal pattern. These findings supcharacteristic features of erythrocytes port the suggestion that juvenile of newborn infants: the fetal hemochronic myelogenous leukemia is acglobin concentration was greatly elecompanied by reversion to a fetal patvated (72#{176}/o); the oxygen dissociation tern of erythropoiesis. curve of the whole blood was disE LEVATED LEVELS of fetal hemoglobin accompany a variety of congenital hematologic disorders. These include hemoglobinopathies, thalassemias, hypoplastic anemias, and the syndromes of hereditary persistence of fetal hemoglobin. The high fetal hemoglobin levels present in the last condition, and to some extent in the others, may represent a congenital abnormality in which the normal switchover from fetal to adult hemoglobin synthesis is incomplete or absent.’ Fetal hemoglobin levels may also be higher than normal in a number of acquired disorders,2 including pernicious anemia, aplastic anemia, myelofibrosis, sideroblastic anemia, paroxysmal nocturnal hemoglobinuria, and several types of leukemia.3 Usually, however, the fetal hemoglobin concentration in acquired hematologic disorders is only moderately increased, falling within the range of 2-12%. A notable exception is the juvenile form of chronic myelogenous leukemia, in which hemoglobin F comprises 30-70% of the total hemoglobin. This form of leukemia is distinguished from the more common adult type by a younger age of onset, the presence of early thrombocytopenia, the absence of a Philadelphia chromosome, and a generally poor response to therapy. In addition to the increased percentages of fetal hemo-