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Probable manifestations of the intrinsic corpuscular defect leading to shortened red blood cell (RBC) survival in hereditary spherocytosis (HS) have been induced by in vitro incubation of these erythrocytes (2-4). The classical in vitro changes that have been described are a marked increase in autohemolysis in the absence of metabolized substrate and an increase in osmotic fragility. Young, Izzo, Altman, and Swisher (4) showed that a number of substrates utilized by RBC to produce ATP could substitute for glucose in preventing the exaggerated in vitro hemolysis in HS erythrocytes. The exact role of cellular ATP in preventing these changes has, however, been debated. Selwyn and Dacie (3) suggested that, particularly in the absence of metabolized substrate, a premature degeneration of the membrane occurred in HS erythrocytes during in vitro incubations. In a preliminary report (1), we described an in vitro loss of lipid in HS erythrocytes not found in normal cells that was minimized, but not prevented completely, by the presence of glucuose. These findings appeared to be a specific manifestation of the membrane degeneration postulated by Selwyn and Dacie (3) and to represent an example of the mechanism, originally proposed by London and Schwartz (5), whereby RBCcellular energy is utilized in preventing changes in membrane lipids; in HS erythrocytes, it appeared that utilization of energy through this pathway was inefficient.

Erythrocyte lipid loss in hereditary spherocytosis.