Kalmanti M, Kalmantis T
First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece.
Pediatr Hematol Oncol. 1989;6(2):85-93. doi: 10.3109/08880018909034274.
In order to investigate the pathogenesis of anemia in childhood malignancy, we studied erythroid cell proliferation responses with bone marrow erythroid cultures and serum erythropoietin (Ep) levels in 32 children with lymphomas and malignant tumors. The erythroid colony formation from 20 normal controls (mean 68.8 colony-forming-unit erythroid [CFU-E] and 32 burst-forming-unit erythroid [BFU-E] derived colonies/10(5) mononuclear cells), was higher than that seen in children with lymphomas (mean 45.9 CFU-E and 20.7 BFU-E/10(5) cells, p less than 0.01) but similar to the values obtained from children with tumors (mean 65.1 CFU-E and 28.1 BFU-E/10(5) mononuclear cells). The degree of anemia in children with lymphomas correlated negatively (r = -0.7, p less than 0.01) with serum Ep levels. In contrast, a weak positive correlation (r = 0.3, p greater than 0.1) was observed between the degree of anemia and Ep values in the group with tumors. We suggest that the decreased number of committed erythroid progenitors in lymphomas may be the main factor for anemia in these patients, while the abnormal response of Ep to the degree of the anemia suggests a defect in erythropoiesis in children with tumors.