• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Liver cirrhosis induced by long-term administration of a daily low dose of amiodarone: a case report.长期每日低剂量服用胺碘酮所致肝硬化:一例报告
World J Gastroenterol. 2005 Sep 14;11(34):5394-7. doi: 10.3748/wjg.v11.i34.5394.
2
Low dose amiodarone causing pseudo-alcoholic cirrhosis.低剂量胺碘酮导致假性酒精性肝硬化。
Age Ageing. 2003 Mar;32(2):224-5. doi: 10.1093/ageing/32.2.224.
3
Hepatic cirrhosis caused by low-dose oral amiodarone therapy.
Am J Med Sci. 2005 Nov;330(5):257-61. doi: 10.1097/00000441-200511000-00012.
4
Amiodarone-induced reversible and irreversible hepatotoxicity: two case reports.胺碘酮所致可逆性和不可逆性肝毒性:两例报告
J Med Case Rep. 2018 Apr 14;12(1):95. doi: 10.1186/s13256-018-1629-8.
5
Amiodarone and cirrhosis.
Age Ageing. 2004 Mar;33(2):207-8; author reply 208. doi: 10.1093/ageing/afh053.
6
Amiodarone-induced liver cirrhosis and parkinsonism: a case report.
Clin Neuropathol. 2010 Mar-Apr;29(2):84-8. doi: 10.5414/npp29084.
7
Amiodarone induced liver cirrhosis. Report of two cases.
J Gastrointestin Liver Dis. 2009 Jun;18(2):233-5.
8
[Pseudo-alcoholic hepatitis and cirrhosis caused by amiodarone (Cordarone)].
Rev Med Liege. 1998 Mar;53(3):121-4.
9
Chronic liver disease after low daily doses of amiodarone. Report of three cases.低日剂量胺碘酮所致慢性肝病。三例报告。
J Hepatol. 1986;3(2):228-32. doi: 10.1016/s0168-8278(86)80031-9.
10
Drug-induced steatohepatitis leading to cirrhosis: long-term toxicity of amiodarone use.药物性脂肪性肝炎导致肝硬化:胺碘酮使用的长期毒性
Semin Liver Dis. 2009 Nov;29(4):423-8. doi: 10.1055/s-0029-1240011. Epub 2009 Oct 13.

引用本文的文献

1
Changes in Hepatic Density Due to Oral Amiodarone-induced Liver injury Shown by Computed Tomography.计算机断层扫描显示口服胺碘酮所致肝损伤引起的肝脏密度变化
Intern Med. 2025 Jun 15;64(12):1828-1833. doi: 10.2169/internalmedicine.4436-24. Epub 2024 Nov 21.
2
Double Hit of Hydroxichloroquine and Amiodarone Induced Renal Phospholipidosis in a Patient with Monoclonal Gammopathy and Sclerodermiform Syndrome: A Case Report and Review of the Literature.羟氯喹和胺碘酮双重打击导致单克隆丙种球蛋白病和硬皮病样综合征患者肾磷脂沉积症:病例报告及文献复习。
Med Sci (Basel). 2024 May 15;12(2):25. doi: 10.3390/medsci12020025.
3
Cell-Based Imaging Assay for Detection of Phospholipidosis.基于细胞的磷脂蓄积检测成像分析方法。
Methods Mol Biol. 2022;2474:73-82. doi: 10.1007/978-1-0716-2213-1_8.
4
Role of immune dysfunction in drug induced liver injury.免疫功能障碍在药物性肝损伤中的作用。
World J Hepatol. 2021 Nov 27;13(11):1677-1687. doi: 10.4254/wjh.v13.i11.1677.
5
Analysis of computed tomography density of liver before and after amiodarone administration.
Jpn J Radiol. 2018 May;36(5):340-344. doi: 10.1007/s11604-018-0733-4. Epub 2018 Apr 2.
6
Definition and risk factors for chronicity following acute idiosyncratic drug-induced liver injury.急性特异质性药物性肝损伤后慢性化的定义及危险因素
J Hepatol. 2016 Sep;65(3):532-42. doi: 10.1016/j.jhep.2016.05.003. Epub 2016 May 13.
7
Identification of hepatic phospholipidosis inducers in sandwich-cultured rat hepatocytes, a physiologically relevant model, reveals altered basolateral uptake and biliary excretion of anionic probe substrates.在具有生理相关性的三明治培养大鼠肝细胞模型中鉴定肝磷脂蓄积诱导物,揭示了阴离子探针底物的基底外侧摄取和胆汁排泄的改变。
Toxicol Sci. 2014 May;139(1):99-107. doi: 10.1093/toxsci/kfu033. Epub 2014 Feb 22.
8
Detection of phospholipidosis induction: a cell-based assay in high-throughput and high-content format.磷脂沉积症诱导的检测:一种高通量和高内涵形式的基于细胞的检测方法。
J Biomol Screen. 2014 Jan;19(1):66-76. doi: 10.1177/1087057113502851. Epub 2013 Sep 3.
9
Amiodarone-induced cirrhosis of liver: what predicts mortality?胺碘酮所致肝硬化:哪些因素可预测死亡率?
ISRN Cardiol. 2013;2013:617943. doi: 10.1155/2013/617943. Epub 2013 Mar 14.
10
Increased density of the liver and amiodarone-associated phospholipidosis.肝脏密度增高与胺碘酮相关性磷脂沉积症。
Cardiol Res Pract. 2009;2009:598940. doi: 10.4061/2009/598940. Epub 2009 Sep 13.

本文引用的文献

1
The potential role of genes in nonalcoholic fatty liver disease.基因在非酒精性脂肪性肝病中的潜在作用。
Clin Liver Dis. 2004 Aug;8(3):673-91, xi. doi: 10.1016/j.cld.2004.04.001.
2
The ins and outs of mitochondrial dysfunction in NASH.非酒精性脂肪性肝炎中线粒体功能障碍的来龙去脉。
Diabetes Metab. 2004 Apr;30(2):121-38. doi: 10.1016/s1262-3636(07)70098-8.
3
Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease.非酒精性脂肪性肝病中肝脏胰岛素抵抗的机制。
J Biol Chem. 2004 Jul 30;279(31):32345-53. doi: 10.1074/jbc.M313478200. Epub 2004 May 27.
4
Inhibition of microsomal triglyceride transfer protein: another mechanism for drug-induced steatosis in mice.微粒体甘油三酯转运蛋白的抑制:小鼠药物性脂肪变性的另一种机制。
Hepatology. 2003 Jul;38(1):133-40. doi: 10.1053/jhep.2003.50309.
5
Low dose amiodarone causing pseudo-alcoholic cirrhosis.低剂量胺碘酮导致假性酒精性肝硬化。
Age Ageing. 2003 Mar;32(2):224-5. doi: 10.1093/ageing/32.2.224.
6
Genetic and epigenetic factors in autoimmune reactions toward cytochrome P4502E1 in alcoholic liver disease.酒精性肝病中针对细胞色素P4502E1自身免疫反应的遗传和表观遗传因素
Hepatology. 2003 Feb;37(2):410-9. doi: 10.1053/jhep.2003.50049.
7
Drugs and steatohepatitis.药物与脂肪性肝炎。
Semin Liver Dis. 2002;22(2):185-94. doi: 10.1055/s-2002-30106.
8
Tumor necrosis factor alpha promoter polymorphisms and insulin resistance in nonalcoholic fatty liver disease.
Gastroenterology. 2002 Feb;122(2):274-80. doi: 10.1053/gast.2002.31065.
9
Interleukin 10 promoter region polymorphisms and susceptibility to advanced alcoholic liver disease.白细胞介素10启动子区域多态性与晚期酒精性肝病易感性
Gut. 2000 Apr;46(4):540-5. doi: 10.1136/gut.46.4.540.
10
Increased hepatic iron concentration in nonalcoholic steatohepatitis is associated with increased fibrosis.
Gastroenterology. 1998 Feb;114(2):311-8. doi: 10.1016/s0016-5085(98)70482-2.

长期每日低剂量服用胺碘酮所致肝硬化:一例报告

Liver cirrhosis induced by long-term administration of a daily low dose of amiodarone: a case report.

作者信息

Oikawa Hiroki, Maesawa Chihaya, Sato Ryo, Oikawa Kanta, Yamada Hiroyuki, Oriso Seizo, Ono Sadahide, Yashima-Abo Akiko, Kotani Koji, Suzuki Kazuyuki, Masuda Tomoyuki

机构信息

Department of Pathology, Iwate Medical University School of Medicine, Uchimaru 19-1, Morioka 020-8505, Japan.

出版信息

World J Gastroenterol. 2005 Sep 14;11(34):5394-7. doi: 10.3748/wjg.v11.i34.5394.

DOI:10.3748/wjg.v11.i34.5394
PMID:16149155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4622818/
Abstract

The anti-arrhythmic agent amiodarone (AD) is associated with numerous adverse effects, but serious liver disease is rare. The improved safety of administration of daily low doses of AD has already been established and this regimen is used for long-term medication. Nevertheless, asymptomatic continuous liver injury by AD may increase the risk of step-wise progression of non-alcoholic fatty liver disease. We present an autopsy case of AD-induced liver cirrhosis in a patient who had been treated with a low dose of AD (200 mg/d) daily for 84 mo. The patient was a 85-year-old male with a history of ischemic heart disease. Seven years after initiation of treatment with AD, he was admitted with cardiac congestion. The total dose of AD was 528 g. Mild elevation of serum aminotransferase and hepatomegaly were present. Liver biopsy specimens revealed cirrhosis, and under electron microscopy numerous lysosomes with electron-dense, whorled, lamellar inclusions characteristic of a secondary phospholipidosis were observed. Initially, withdrawal of AD led to a slight improvement of serum aminotransferase levels, but unfortunately his general condition deteriorated and he died from complications of pneumonia and renal failure. Long-term administration of daily low doses of AD carries the risk of progression to irreversible liver injury. Therefore, periodic examination of liver function and/or liver biopsy is required for the management of patients receiving long-term treatment with AD.

摘要

抗心律失常药物胺碘酮(AD)会引发多种不良反应,但严重肝病较为罕见。每日低剂量服用AD的安全性已得到改善,该方案用于长期用药。然而,AD导致的无症状持续性肝损伤可能会增加非酒精性脂肪性肝病逐步进展的风险。我们报告一例AD诱发肝硬化的尸检病例,该患者每日服用低剂量AD(200mg/d),共84个月。患者为85岁男性,有缺血性心脏病史。开始服用AD七年后,他因心脏充血入院。AD的总剂量为528g。血清转氨酶轻度升高,肝脏肿大。肝活检标本显示肝硬化,电子显微镜下观察到大量溶酶体,其具有电子致密、漩涡状、层状包涵体,这是继发性磷脂沉积症的特征。最初,停用AD后血清转氨酶水平略有改善,但不幸的是,他的全身状况恶化,死于肺炎和肾衰竭并发症。长期每日低剂量服用AD存在进展为不可逆肝损伤的风险。因此,对于接受AD长期治疗的患者,需要定期检查肝功能和/或进行肝活检。