Ascorbic-acid-induced haemolysis in G-6-PD deficiency.

THOUGH THE ORIGINS of erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency are rooted in human antiquity, the presence of drug-induced hemolysis in individuals subsequently felt to have G-6-PD deficiency was first reported in 1926 and the biochemical lesion responsible for this phenomenon elucidated in 1956 (1). In the United States, hemolysis induced by infection or drugs is the most common clinical manifestation of G-6-PD deficiency (2). Ascorbic acid (vitamin C), an essential vitamin, is commonly used in pharmacologic doses for the prevention of the common cold and to promote the healing of wounds. We report here an individual with G-6-PD deficiency who developed intravascular hemolysis and acute renal failure after being treated with large amounts of ascorbic acid. The G-6-PD isoenzyme present in the vast majority of people of African descent with G-6-PD deficiency, GdA-, is characterized by rapid electrophoretic mobility, moderate deficiency in activity, and increased in-vivo lability (2). The details of the procedures used for the detection of G6-PD deficiency have been previously described (3).