Zimmerman H J
Arch Intern Med. 1981 Feb 23;141(3 Spec No):333-42. doi: 10.1001/archinte.141.3.333.
The mechanism for aspirin-caused liver injury is not clear. Aspirin produces hepatotoxic reactions as a cumulative phenomenon, requiring days or weeks to develop. Patients with active rheumatic or collagen disease, as well as children, are especially susceptible. Blood levels of salicylate higher than 25 mg/dL are particularly likely to lead to hepatic injury. Levels lower than 15 mg/dL rarely do. The mechanism for acetaminophen liver damage is quite clear. It produces hepatic injury as a result of a large single overdose, usually suicidal in intent. Patients with acetaminophen blood levels higher than 300 mg/dL at four hours after intake are most likely to develop hepatic damage; when N-acetylcysteine is used within the first ten hours after ingestion of an overdose, the recovery rate is reported to be virtually 100%. The conditions of patients receiving long-term full doses of either aspirin or acetaminophen should be intermittently monitored for hepatic injury.
阿司匹林导致肝损伤的机制尚不清楚。阿司匹林引发肝毒性反应是一种累积现象,需要数天或数周时间才会显现。患有活动性风湿或胶原病的患者以及儿童尤其易感。水杨酸盐血药浓度高于25mg/dL时特别容易导致肝损伤。低于15mg/dL时则很少会导致肝损伤。对乙酰氨基酚肝损伤的机制相当明确。它是由于单次大量服药过量(通常有自杀意图)而造成肝损伤。服药四小时后血药浓度高于300mg/dL的对乙酰氨基酚患者最有可能发生肝损伤;据报道,在过量服药后前十小时内使用N-乙酰半胱氨酸,恢复率几乎可达100%。应定期监测长期服用全剂量阿司匹林或对乙酰氨基酚患者的肝损伤情况。