Crippin J S
Liver Service, Baylor University Medical Center, Dallas, Texas.
Am J Gastroenterol. 1993 Apr;88(4):590-2.
Potentiation of acetaminophen hepatotoxicity has previously been associated with a history of alcohol abuse. Presented here is the case of a 21-yr-old Philippino female with rapidly deteriorating hepatic functions. She had been on isoniazid, 300 mg daily, as prophylaxis against tuberculosis due to a positive tuberculin skin test. She took 3.25 g of acetaminophen for abdominal cramping and subsequently had rapid deterioration of liver function manifested by prolongation of the prothrombin time, elevated ammonia, marked elevation of transaminases, and hyperbilirubinemia. Over the course of 1 wk, these values essentially normalized and she was discharged. Isoniazid induces the cytochrome P-450 system, resulting in increased metabolism of acetaminophen, formation of toxic metabolites, depletion of glutathione stores, and subsequent hepatocellular injury. Patients on isoniazid should use caution when taking acetaminophen since the potentially hepatotoxic effects may be amplified due to induction of the cytochrome P-450 system.
对乙酰氨基酚肝毒性的增强此前一直与酒精滥用史有关。本文介绍了一名21岁菲律宾女性肝功能迅速恶化的病例。她因结核菌素皮肤试验呈阳性，每天服用300毫克异烟肼以预防结核病。她因腹部绞痛服用了3.25克对乙酰氨基酚，随后出现肝功能迅速恶化，表现为凝血酶原时间延长、血氨升高、转氨酶显著升高和高胆红素血症。在1周内，这些指标基本恢复正常，她出院了。异烟肼诱导细胞色素P-450系统，导致对乙酰氨基酚代谢增加、有毒代谢物形成、谷胱甘肽储备耗竭以及随后的肝细胞损伤。服用异烟肼的患者在服用对乙酰氨基酚时应谨慎，因为细胞色素P-450系统的诱导可能会放大潜在的肝毒性作用。
