In view of the erythroid hyperplasia found in the bone marrow of subjects with chronic iron deficiency anemia, the delayed appearance of reticulocytosis following iron therapy is unexplained. Profound disturbances were observed in some biochemical functions of the bone marrow cells isolated from such patients. There was a substantial decrease in the cellular nucleic acid content, associated with a marked drop in the rate of 3H-thymidine incorporation into DNA. The utilization of 59iron and of glycine-2-14C for heme production, and of the latter compound for protein synthesis was also reduced, as compared to the findings in bone marrow cells from normal subjects. These metabolic alterations returned to the normal pattern in the bone marrow cell suspensions obtained from the patients following recovery after iron therapy.

The possible implications of these findings are discussed in the light of available information.

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