中国药物警戒 ›› 2015, Vol. 12 ›› Issue (6): 347-351.

• 药械安全性研究 • 上一篇    下一篇

60例静脉滴注盐酸胺碘酮致急性肝损害病例分析

毛敏1,徐小华1,赵嘉澍1,1,毛建生3,杜金行3,陆进1   

  1. 1中日友好医院药学部,北京 100029;
    2普仁医院药学部,北京 100062;
    3中日友好医院中西医结合心内科,北京 100029
  • 收稿日期:2014-07-30 出版日期:2015-06-08 发布日期:2015-07-27
  • 作者简介:毛敏,男,硕士,主管药师,中西医结合心内科临床药学。

Analysis of 60 Cases of Acute Hepatic Injury Induced by Intravenous Infusion of Amiodarone

MAO Min1,XU Xiao-hua1,ZHAO Jia-shu1,2,MAO Jian-sheng3,DU Jin-hang3, LU Jin1   

  1. 1Department of Pharmacy, China-Japan Friendship Hospital, Beijing 100029, China;
    2Department of Pharmacy, Puren Hospital, Beijing 100062, China;
    3Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100062, China
  • Received:2014-07-30 Online:2015-06-08 Published:2015-07-27

摘要: 目的 总结静脉滴注胺碘酮致急性肝损害的病例特点,分析其发生的原因和机制,并探讨防治办法。方法 对我院2011年发生的1例以及1988~2012年国内外文献报道的59例静脉滴注胺碘酮后出现急性肝损害患者的基本情况、基础疾病、胺碘酮应用指征及使用方法 、肝功能损害特点及其他器官功能、合并用药情况以及转归等进行分析。结果 急性肝损害前静脉滴注胺碘酮剂量为193.2~4 310(1 345.7±550.6)mg,用药至发现肝损害的时间为6~96(34.0±17.9)h,天冬氨酸氨基转移酶峰值为122.3~17 471(3 798±3 982)U?L-1,丙氨酸氨基转移酶峰值为225~12 426(3 206±1 788)U?L-1。停用胺碘酮注射液及常规肝脏辅助治疗后,52例患者肝酶降至正常的平均时间为21.6±13.24 d,4例因急性肾功能不全或多脏器功能衰竭死亡,1例因肝性脑病死亡,3例因心源性休克死亡。15例患者改为口服胺碘酮,肝功能继续趋于好转。结论 静脉胺碘酮急性肝损害的发生与胺碘酮用药总量及疗程之间的关系暂不明确,而高浓度的助溶剂聚山梨醇酯80是导致急性肝损害最关键的因素。存在其他器官损害的急性肝损害患者预后较差,在治疗早期同时启动静脉制剂与口服制剂便于急性肝损害的处理。当合并急性肾功能衰竭时死亡率高,及早进行连续性血液净化(CBP)有利于救治。

关键词: 胺碘酮, 急性肝损害, 静脉滴注, 不良反应。

Abstract: Objective To conclude intravenous infusion of amiodarone-induced acute hepatic injury cases, to analyze the causal factors and mechanisms of acute hepatic injury induced by intravenous infusion of amiodarone, and to find the way of prevention and treatment of acute hepatic injury. Methods The clinical feature, primary disease, indications and Methods of using amiodarone, characteristics of hepatic injury and functions of other organs, concomitant medicines and prognosis of patients were analyzed in 60 cases. One of the cases was the inpatient of our hospital in 2011, and the others were collected from foreign and domestic medical journals between 1988 to 2012. Results The dosage of intravenous amiodarone was 193.2~4 310(1 345.7±550.6)mg, the duration of administration was 6~29(34.0±17.9)h. The peak of AST was 122.3~17 471(3 798±3 982)U?L-1 and ALT was 225~12 426(3 206±1 788)U?L-1. After discontinuation of intravenous amiodarone and conventional liver adjuvant therapy, 52 cases of liver enzymes returned to normal, the average time was 21.6 ± 13.24 d, 4 cases died of acute renal failure or multi-organ failure, one case died of hepatic encephalopathy, three cases died of cardiogenic shock. The liver function of 15 cases who adopted oral amiodarone after stopping intravenous amiodarone continued to improve. Conclusion The relationship between incidence of acute liver injury induced by intravenous amiodarone and the total does of amiodarone, and the treatment time is unclear. However,the high concentration of cosolvent polysorbate 80 is the most critical factors to lead to acute liver injury. The patient with both acute liver injury and other organs damage would have poor prognosis. Intravenous infusion of amiodarone could be safely replaced by oral amiodarone when acute hepatic injury happened. Acute hepatic injury with acute renal failure induced high mortality, CBP is conducive to treatment as soon as possible.

Key words: amiodarone, acute hepatotoxicity, intravenous administration, adverse reactions

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