Zimmerman H J, Ishak K G
Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
Gastroenterol Clin North Am. 1995 Dec;24(4):739-57.
Medicinal agents can produce various types of hepatic injury by several mechanisms. Hepatic injury may lead to acute syndromes that resemble viral hepatitis, fatty liver of pregnancy, and obstructive jaundice, as well as to a number of chronic syndromes. Acute liver damage relates, at least in part, to the apparent mechanism of injury. Hepatic injury induced by large single overdose of intrinsically toxic drugs (e.g., acetaminophen, ferrous salts) develops within 24 to 72 hours of intake and usually is accompanied by renal failure. Regular intake of some toxic drugs, (e.g., methotrexate) leads to slowly evolving chronic disease. Liver damage due to hypersensitivity-type idiosyncrasy usually appears after 1 to 5 weeks of taking the drug unless there has been previous exposure and is preceded or accompanied by systemic features that are hallmarks of hypersensitivity. Hepatic injury attributable to metabolic idiosyncrasy may appear after weeks to months of taking the drug and usually presents without the systemic features. Organs other than the liver may be involved in the syndrome of drug-induced injury as the result of selective injury or as part of a hypersensitivity reaction.
药物可通过多种机制导致各种类型的肝损伤。肝损伤可能引发类似于病毒性肝炎、妊娠脂肪肝和阻塞性黄疸的急性综合征，以及多种慢性综合征。急性肝损伤至少部分与明显的损伤机制有关。单次大剂量服用本质上有毒的药物（如对乙酰氨基酚、亚铁盐）所引起的肝损伤在服药后24至72小时内出现，通常伴有肾衰竭。长期服用某些有毒药物（如甲氨蝶呤）会导致疾病缓慢进展。超敏反应型特异质性肝损伤通常在服药1至5周后出现，除非之前有过接触，且在出现肝损伤之前或同时伴有超敏反应的全身性特征。代谢特异质性所致的肝损伤可能在服药数周或数月后出现，且通常无全身性特征。作为选择性损伤的结果或作为超敏反应的一部分，药物性损伤综合征可能累及肝脏以外的器官。
