Lavelle K J, Atkinson K F, Kleit S A
Am J Med Sci. 1976 Sep-Oct;272(2):201-4. doi: 10.1097/00000441-197609000-00010.
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 The drug was withdrawn and the hyperlactatemia subsided in three days without specific treatment.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.
一名69岁的葡萄糖-6-磷酸脱氢酶缺乏症男性因脓尿接受了呋喃妥因治疗。四天后，他出现了因乳酸过多导致的代谢性酸中毒、循环血红蛋白下降、网织红细胞增多、血清转氨酶水平升高和高胆红素血症。停用该药物后，高乳酸血症在三天内消退，未进行特殊治疗。在体外，呋喃妥因能够刺激红细胞葡萄糖利用并产生乳酸，同时抑制还原型谷胱甘肽的生成。在体内，这种药物能够在易感个体中引起溶血和肝细胞损伤。药物摄入与溶血、葡萄糖利用增加、乳酸过多以及肝功能不全在时间上的接近表明，呋喃妥因可能是导致所观察到的临床和化学异常的原因。
