胺碘酮引起的肝损伤

Ⅲ类抗心律失常药胺碘酮可引起肝损伤，发生率约为14%-82%。胺碘酮致肝损伤的临床表现差异较大，包括无症状性肝酶水平升高、暴发性肝衰竭甚至死亡。组织病理学表现类似于酒精性肝病，特点为溶酶体内磷脂沉积和颗粒细胞聚集。胺碘酮引起肝损伤的机制主要与药物及其代谢产物的毒性作用、免疫介导和遗传因素相关，静脉给药引起肝损伤主要考虑为助溶剂聚山梨醇酯80作用。男性、心功能不全、血药浓度〉2.5 mg/ L 可能为胺碘酮致肝损伤的危险因素。临床应用胺碘酮应严格掌握适应证，并应根据患者的身体状况选择恰当的用药方法。用药期间应严密监测患者肝功能和/或血药浓度。出现肝功能异常时，应仔细权衡治疗获益和风险而决定是否减量或停药。

Amiodarone-induced hepatic injury

Amiodarone,one of Class Ⅲ antiarrhythmic drugs,may lead to hepatic injury,the incidence of which is about 14% to 82% . Clinical manifestations differ widely from asymptomatic elevated liver enzymes to fulminant hepatic failure and even death. Histopathological findings are similar to those of alcoholic liver disease and characterized by lysosomes phospholipidosis and granular cells. Pathogenesis includes toxicity of amiodarone and its major metabolite,immunological mechanisms,and genetic factors. Intravenous AIHI is mainly related to the effect of cosolvent,polysorbate 80. Men,heart failure and plasma concentration 〉2.5 mg/ L may be risk factors. Indications to use amiodarone should be strictly controlled and patients＇ physical conditions should be considered for choosing methods of administration. Monitoring closely is needed for liver function and/ or blood concentration during treatment. When liver function is abnormal, weigh the benefits and risks of treatment carefully,and decide whether dosage reduction or withdrawal of the drug is necessary.