Abstract
PREVIOUS investigations of drug-induced and fava bean-induced haemolytic anaemia in subjects with a deficiency of glucose-6-phosphate dehydrogenase (G-6-PD) have demonstrated that they are similar both in their clinical characteristics and in the mechanism of genetic transmission of the enzyme defect. Nevertheless, a considerable amount of evidence has accumulated to indicate that this enzyme defect reflects heterogeneous genetic mechanisms in various ethnic groups. It has been demonstrated that the enzyme deficiency may be complete or intermediate, that it may affect erythrocytes alone or involve other tissues1–3, and that the enzyme protein may differ in its characteristics in cells from subjects of different ethnic groups3–7—including its electrophoretic behaviour.
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