Abstract

Based on our experience of a G6PD deficient patient with recurrent episodes of severe hemolysis associated with plymbism, we studied the effect of lead on erythrocytes from 3 normal and 4 stable G6PD deficient patients (3 with A-, 1 with B- variants). RBC's were washed, resuspended 5% v/v in culture medium, incubated for 2 hours at 37°C with lead acetate and/or phenylhydrazine (PH), and the percentage hemolysis determined. At concentrations tested (10-80ug/100ml) lead caused hemolysis only in the G6PD deficient cells. For example, normal RBC's demonstrated .60 ±.10% hemolysis in the absence of lead and .53 ± .05% in its presence (40ug/100ml); G6PD deficient RBC's showed .69 ± .05% and 2.11 ±.57% hemolysis under similar conditions, p<.001. When cells were exposed to PH (0.5mg/ml) as an oxidant stress, the additional presence of lead (40ug/100ml) significantly exacerbated (p<.01) the resultant hemolysis in the G6PD deficient cells: We conclude that lead, at levels seen in minimally poisoned children, represents a heretofore unrecognized hemolytic stimulus in G6PD deficiency. Since the incidence of G6PD deficiency is high in children at risk for plumbism, it is important to recognize lead as being capable of both causing and exacerbating hemolytic crises in these patients.

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