Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion.
A 69-year-old man with glucose-6-phosphate dehydrogenase deficiency was treated with nitrofurantoin for pyuria. Four days later he presented with metabolic acidosis due to excess lactic acid, a decline in curculating hemoglobin, reticulocytosis, elevated serum transaminase levels, and hyperbilirubinemia. The drug was withdrawn and the hyperlactatemia subsided in three days without specific treatment. In vitro, nitrofurantoin is capable of stimulating erythrocyte glucose utilization aand lactate production, and inhibiting the generation of reduced glutathione. In vivo, this drug is capable of producing hemolysis in susceptible subjects and hepatocellular injury. The temporal proximity of drug ingestion and hemolysis, increased glucose utilization, lactate excess, and hepatic insufficiency suggests that nitrofurantoin may have been responisble for precipitating the clinical and chemical abnormalities observed.
Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion. A 69-year-old man with glucose-6-phosphate dehydrogenase deficiency was treated with nitrofurantoin for pyuria. Four days later he presented with metabolic acidosis due to excess lactic acid, a decline in curculating hemoglobin, reticulocytosis, elevated serum transaminase levels, and hyperbilirubinemia. The drug was withdrawn and the hyperlactatemia subsided in three days without specific treatment. In vitro, nitrofurantoin is capable of stimulating erythrocyte glucose utilization aand lactate production, and inhibiting the generation of reduced glutathione. In vivo, this drug is capable of producing hemolysis in susceptible subjects and hepatocellular injury. The temporal proximity of drug ingestion and hemolysis, increased glucose utilization, lactate excess, and hepatic insufficiency suggests that nitrofurantoin may have been responisble for precipitating the clinical and chemical abnormalities observed.