Abstract

Red blood cell survival was estimated in 38 children with nutritional iron deficiency anemia, using Cr51 sodium chromate. Decreased red cell survival was demonstrated in 24 (63 per cent) and appeared to be related to the severity of the anemia and the presence of a functioning spleen. Iron-deficient cells transfused into a splenectomized individual survived normally. A progressive increase in red cell hexokinase activity (without reticulocytosis) was noted in association with increasing severity of anemia and decreasing red cell life span. No such correlation was noted with respect to glucose-6-phosphate dehydrogenase activity or glutathione concentration. Red cell adenosine triphosphate concentration was normal or slightly decreased and showed marked instability on incubation. The role of the spleen in relationship to the metabolic alterations and survival of iron-deficient red cells is discussed. It is suggested that iron-deficient cells would be particularly vulnerable to a reduction in pH or glucose deprivation in the splenic environment, a situation which would be exaggerated in the most severely anemic patients with the greatest increase in red cell hexokinase activity. Red blood cell survival was estimated in 38 children with nutritional iron deficiency anemia, using Cr51 sodium chromate. Decreased red cell survival was demonstrated in 24 (63 per cent) and appeared to be related to the severity of the anemia and the presence of a functioning spleen. Iron-deficient cells transfused into a splenectomized individual survived normally. A progressive increase in red cell hexokinase activity (without reticulocytosis) was noted in association with increasing severity of anemia and decreasing red cell life span. No such correlation was noted with respect to glucose-6-phosphate dehydrogenase activity or glutathione concentration. Red cell adenosine triphosphate concentration was normal or slightly decreased and showed marked instability on incubation. The role of the spleen in relationship to the metabolic alterations and survival of iron-deficient red cells is discussed. It is suggested that iron-deficient cells would be particularly vulnerable to a reduction in pH or glucose deprivation in the splenic environment, a situation which would be exaggerated in the most severely anemic patients with the greatest increase in red cell hexokinase activity.

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