Zimmerman H J
Hepatic Department, Armed Forces Institute of Pathology, Washington, D.C.
Dis Mon. 1993 Oct;39(10):675-787.
Chemical hepatic injury may result from accidental or suicidal exposure to toxic agents in the home or at work or from adverse reactions to medicinal agents. Chemical hepatic injury can lead to acute or chronic syndromes. Acute injury may be cytotoxic, cholestatic, or mixed. Cytotoxic injury is characterized by necrosis, steatosis, or both. Cholestatic injury is characterized by arrested bile flow and may be associated with portal inflammation or may occur in a setting in which there is no evidence of inflammation. Chronic hepatic injury includes chronic active hepatitis, steatosis, phospholipidosis, veno-occlusive disease, several forms of cirrhosis, peliosis hepatis, and hepatic neoplasms. The mechanism for injury may be intrinsic toxicity of the agent, reaction of an unusually susceptible host, or a combination of the two factors. Unusual susceptibility may be the result of immunologic idiosyncrasy (hypersensitivity reaction) or injury from a toxic metabolite (metabolic idiosyncrasy) of the drug.
化学性肝损伤可能源于在家中或工作场所意外或自杀性接触有毒物质，或药物的不良反应。化学性肝损伤可导致急性或慢性综合征。急性损伤可能是细胞毒性、胆汁淤积性或混合性的。细胞毒性损伤的特征是坏死、脂肪变性或两者皆有。胆汁淤积性损伤的特征是胆汁流动受阻，可能与门静脉炎症相关，或可能发生在无炎症证据的情况下。慢性肝损伤包括慢性活动性肝炎、脂肪变性、磷脂沉着症、肝静脉闭塞病、多种形式的肝硬化、肝紫癜和肝肿瘤。损伤机制可能是药物本身的内在毒性、异常易感宿主的反应或这两个因素的组合。异常易感性可能是免疫特异反应（过敏反应）或药物有毒代谢产物所致损伤（代谢特异反应）的结果。
