Chan A L F, Hsieh H J, Hsieh Y-A, Lin S-J
Department of Pharmacy, Chi Mei Medical Center, Tainan, Taiwan.
Int J Clin Pharmacol Ther. 2008 Feb;46(2):96-101. doi: 10.5414/cpp46096.
To report a fatal case of amiodarone-induced acute hepatotoxicity after intravenous amiodarone administration and similar fatal cases review.
A 72-year-old woman with a history of hypertension, prior cardiovascular disease, atrial fibrillation and diabetes mellitus was admitted to the hospital with acute pyelonephritis and transferred to the intensive care unit due to cerebral infarction. An antidiabetic drug, a low dose of aspirin and intravenous amiodarone therapy was started. After receiving a second dose of amiodarone (1,200 mg; injection rate 1 mg/min), the woman developed ascites, jaundice, high levels of serum transaminases, decreased prothrombin time, and finally became unconscious. Immediately after treatment was discontinued, her extremely high hepatic parameters returned to normal. According to the Naranjo probability scale, this adverse reaction was highly probable.
The occurrence of acute liver damage after intravenous amiodarone is rare but harmful. It can be induced by polysorbate 80, a solubilizer, by immunomediated centrilobular necrosis, or by the presence of a functional PPAR-I+/- gene.
Amiodarone is an effective antiarrhythmic agent for preventing and treating atrial and ventricular arrhythmias. The molecular mechanism causing acute hepatic damage after amiodarone treatment is not clear. Therefore, amiodarone must be administered with care, and liver function should be monitored closely in patients treated with this drug.
报告1例静脉注射胺碘酮后发生胺碘酮诱导的急性肝毒性致死病例并回顾类似致死病例。
一名72岁女性，有高血压、既往心血管疾病、心房颤动和糖尿病病史，因急性肾盂肾炎入院，后因脑梗死转入重症监护病房。开始使用一种抗糖尿病药物、低剂量阿司匹林和静脉注射胺碘酮治疗。在接受第二剂胺碘酮（1200mg；注射速率1mg/min）后，该女性出现腹水、黄疸、血清转氨酶水平升高、凝血酶原时间缩短，最终昏迷。治疗停止后，其极高的肝脏指标立即恢复正常。根据Naranjo概率量表，这种不良反应很可能发生。
静脉注射胺碘酮后发生急性肝损伤虽罕见但有害。它可由增溶剂聚山梨酯80、免疫介导的小叶中心坏死或功能性PPAR-I+/-基因的存在诱发。
胺碘酮是预防和治疗心房及心室心律失常的有效抗心律失常药物。胺碘酮治疗后引起急性肝损伤的分子机制尚不清楚。因此，使用胺碘酮时必须谨慎，并应密切监测接受该药物治疗患者的肝功能。
