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一个致命后果:胺碘酮诱发的多器官毒性。

A Fatal Consequence: Amiodarone-Induced Multiorgan Toxicity.

作者信息

Al-Hiari Mohammed, Abumuhfouz Ma'in, Kayali Leen, Panta Utsab, Rueda Rios Carlos

机构信息

Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, USA.

Internal Medicine, University of Missouri Kansas City, Kansas City, USA.

出版信息

Cureus. 2024 Jun 12;16(6):e62260. doi: 10.7759/cureus.62260. eCollection 2024 Jun.

DOI:10.7759/cureus.62260
PMID:39006582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11245305/
Abstract

Amiodarone is commonly used nowadays for the treatment of atrial fibrillation (AF). The wide use of this medication has led to the occurrence of adverse events, including pulmonary toxicity, hepatotoxicity, thyroid dysfunction, and many others. Higher doses of Amiodarone of ≥400 mg/day have been linked to increased complications. We present a case of a 70-year-old male with multivessel coronary artery disease (CAD) with ischemic cardiomyopathy and severe peripheral artery disease (PAD) who underwent an elective left femoral to posterior tibial bypass surgery followed by percutaneous coronary intervention (PCI) complicated by new-onset AF. The patient was loaded with 150 mg of intravenous (IV) Amiodarone followed by 360 mg infusion over six hours for chemical cardioversion. The patient was then maintained on oral Amiodarone 400 mg/day until the day of presentation when he complained of progressive dyspnea. Imaging was significant for diffuse ground glass opacities and interstitial thickening. The echocardiogram revealed an improved ejection fraction (EF) of 40% from 20%. The patient had worsening oxygenation despite adequate IV diuresis and developed severe acute respiratory distress syndrome (ARDS) requiring mechanical ventilation (MV). A bronchoscopy with bronchoalveolar lavage (BAL) showed diffuse alveolar hemorrhage (DAH) with a high lymphocyte count and negative infectious disease testing. Lab tests revealed elevated liver enzyme levels. There were also changes in thyroid function from baseline with elevated free T4 at 1.83 ng/dL (0.8-1.4 ng/dL), suppressed thyroid stimulating hormone (TSH) at 0.109 mIU/mL (0.4-4 mIU/mL), negative anti-thyroglobulin (TG) antibodies, and anti-thyroid peroxidase (TPO) antibodies indicating a type 2 Amiodarone-induced thyrotoxicosis. Unfortunately, the patient's condition deteriorated further despite appropriate treatment, and it was ultimately followed by his demise. Severe, fatal cases of Amiodarone toxicity are scarce, but more reports are being seen. We strongly believe clinicians should have a high index of suspicion for Amiodarone-related adverse events in elderly males with cardiopulmonary comorbidities. It is imperative to have an increased understanding, greater vigilance, and closer monitoring of pulmonary function tests (PFTs), laboratory tests, and imaging studies.

摘要

胺碘酮如今常用于治疗心房颤动(AF)。这种药物的广泛使用导致了不良事件的发生,包括肺毒性、肝毒性、甲状腺功能障碍等诸多情况。每日剂量≥400毫克的高剂量胺碘酮与并发症增加有关。我们报告一例70岁男性病例,该患者患有多支冠状动脉疾病(CAD)并伴有缺血性心肌病和严重外周动脉疾病(PAD),他接受了择期左股动脉至胫后动脉搭桥手术,随后进行经皮冠状动脉介入治疗(PCI),术后并发新发房颤。患者静脉注射150毫克胺碘酮进行负荷给药,随后在6小时内输注360毫克以进行化学复律。然后患者维持口服胺碘酮400毫克/天,直到他出现进行性呼吸困难前来就诊。影像学检查显示弥漫性磨玻璃影和间质增厚。超声心动图显示射血分数(EF)从20%提高到了40%。尽管进行了充分的静脉利尿治疗,但患者的氧合情况仍在恶化,并发展为严重的急性呼吸窘迫综合征(ARDS),需要机械通气(MV)。支气管镜检查及支气管肺泡灌洗(BAL)显示弥漫性肺泡出血(DAH),淋巴细胞计数高,传染病检测呈阴性。实验室检查显示肝酶水平升高。甲状腺功能也与基线相比发生了变化,游离T4升高至1.83纳克/分升(0.8 - 1.4纳克/分升),促甲状腺激素(TSH)被抑制至0.109毫国际单位/毫升(0.4 - 4毫国际单位/毫升),抗甲状腺球蛋白(TG)抗体和抗甲状腺过氧化物酶(TPO)抗体均为阴性,提示为2型胺碘酮所致甲状腺毒症。不幸的是,尽管进行了适当治疗,患者的病情仍进一步恶化,最终死亡。严重的、致命的胺碘酮毒性病例较为罕见,但此类报告正逐渐增多。我们坚信临床医生对于患有心肺合并症的老年男性患者发生的与胺碘酮相关的不良事件应保持高度怀疑。必须加强对肺功能测试(PFT)、实验室检查和影像学研究的理解、提高警惕并密切监测。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/f9b6f892e997/cureus-0016-00000062260-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/0fa6e15b5fdd/cureus-0016-00000062260-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/3927c99f7c30/cureus-0016-00000062260-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/aaa0d3084e86/cureus-0016-00000062260-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/775469fc013f/cureus-0016-00000062260-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/f9b6f892e997/cureus-0016-00000062260-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/0fa6e15b5fdd/cureus-0016-00000062260-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/3927c99f7c30/cureus-0016-00000062260-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/aaa0d3084e86/cureus-0016-00000062260-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/775469fc013f/cureus-0016-00000062260-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f8f/11245305/f9b6f892e997/cureus-0016-00000062260-i07.jpg

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