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A hereditary abnormality of the erythrocytes was described in Negroes sensitive to primaquine (1). A similar or identical defect has been detected in the erythrocytes of a considerable proportion of non-Ashkenazic Jews susceptible to favism and sensitive to various drugs (2-4). The primary defect of these erythrocytes is probably the markedly decreased activity of glucose6-phosphate dehydrogenase (5). The cells, however, demonstrate a multitude of secondary abnormalities, namely: a low glutathione (GSH) level; glutathione instability; a decreased glycine incorporation rate into GSHin vitro; and an increase in glutathione reductase, aldolase and triphosphopyridine nucleotide (6-9). This hereditary erythrocyte defect is transmitted probably as a sex-linked incompletely dominant trait with various degrees of expressivity of the abnormal gene in affected females (3, 10). In view of the importance of the hexose monophosphate shunt in glucose metabolism in various tissues and the key role of glucose-6-phosphate dehydrogenase in this metabolic pathway, it is of great interest to determine whether this genetic defect of the erythrocytes is demonstrable in other tissues of the affected subjects. In the present communication we describe the results of an investigation of glucose-6-phosphate dehydrogenase activity in platelets of normal and affected individuals.

A STUDY OF SUBJECTS WITH ERYTHROCYTE GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY: INVESTIGATION OF PLATELET ENZYMES*