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Increased osmotic and mechanical fragility of the erythrocytes is a consistent finding in patients with hereditary spherocytosis, although in a few individuals it is necessary to incubate the cells at 370 C. for 24 hours before the otherwise latent abnormality becomes demonstrable. Splenectomy will correct the hemolytic process of hereditary spherocytosis despite the continuing production of abnormally fragile cells by the patient. The spleen is, therefore, essential in the destruction of the intrinsically defective erythrocytes. In the peripheral blood of some individuals with this disease a "double population" of cells exists. One component consists of more markedly fragile cells that are not present after splenectomy and must, therefore, have been related to the presence of the spleen. The present study was undertaken to investigate the changes in osmotic and mechanical fragility accompanying in vivo erythrocyte aging and splenic sequestration and to elucidate the source and fate of the more markedly fragile group of red cells found in some patients. Advantage was taken of the increased erythropoiesis in patients with hereditary spherocytosis prior to splenectomy to label in vivo with Fe59 the new red cells produced during a short time span, thereby obtaining an identifiable group of cells of known age. Using techniques that will be described, it was possible to differentiate these isotopically-labeled cells from the other cells in the peripheral circulation and to compare their char

ALTERATIONS IN OSMOTIC AND MECHANICAL FRAGILITY RELATED TO IN VIVO ERYTHROCYTE AGING AND SPLENIC SEQUESTRATION IN HEREDITARY SPHEROCYTOSIS*†