Amiodarone-Induced Multi-Systemic Toxicity Involving the Liver, Lungs, Thyroid, and Eyes: A Case Report

Frontiers in Cardiovascular Medicine

article

Hye-Su You¹  Jae Hyun Yoon¹  Sung Bum Cho²  Yoo-Duk Choi³  Yung Hui Kim⁴  Wonsuk Choi⁵  Ho-Cheol Kang⁵  Sung Kyu Choi¹ 

[1] Department of Gastroenterology and Hepatology, Chonnam National University Hospital and Medical School;Department of Gastroenterology and Hepatology, Hwasun Chonnam National University Hospital and Medical School;Department of Pathology, Chonnam National University Hospital and Medical School;Department of Ophthalmology, Chonnam National University Hospital and Medical School;Department of Endocrinology, Hwasun Chonnam National University Hospital and Medical School

关键词: amiodarone;    toxicity;    liver;    lung;    thyroid;   

DOI  :  10.3389/fcvm.2022.839441

学科分类：地球科学(综合)

来源: Frontiers

【 摘 要 】

Objectives Amiodarone is widely used to treat arrhythmia. However, amiodarone is known for its severe toxicity to the liver, lungs, and thyroid. Amiodarone causes liver damage ranging from asymptomatic serum aminotransferase elevation to hepatic failure requiring liver transplantation. Although amiodarone toxicity has been reported, its simultaneous multi-organ toxicity is not well-known. Here, we introduce a novel case of multi-systemic amiodarone toxicity involving the liver, lungs, thyroid, and eyes. Case Presentation A 61-year-old woman visited the emergency room due to general weakness, nausea, visual disturbance, heat intolerance, and a non-productive cough. The patient had been using clopidogrel and amiodarone due to underlying atrial fibrillation. The total level of bilirubin was 0.71 mg/dL, aspartate aminotransferase was 358 U/L, alanine aminotransferase was 177 U/L, and prothrombin time was 27.1 s. Computed tomography showed diffuse increased liver intensity and scattered hyperattenuated nodular consolidations in both lungs. Transthoracic needle lung biopsy revealed fibrinoid interstitial inflammation with atypical change of type II pneumocytes and intra-alveolar foamy macrophages. In addition, the thyroid-stimulating hormone level was <0.008 μIU/mL, and free thyroxine was 4.67 ng/dL. The thyroid scan showed diffuse homogenous intake of technetium-99 m pertechnetate in both thyroid lobes. The ophthalmologic exam detected bilateral symmetrical corneal deposits in a vortex pattern. With these findings, we could diagnose amiodarone-induced hepatic, pulmonary, thyroid, and ophthalmologic toxicity. Liver function was restored after cessation of amiodarone, and thyroid function was normalized with methimazole administration. However, due to aggravated lung consolidations, systemic steroid treatment was administered, and improvement was seen 1 week after, at the follow-up exam. As her symptoms improved, she was discharged with a plan of steroid administration for 3 to 6 months. Conclusions This case implies the possibility of multi-systemic amiodarone toxicity. Thus, the toxicity of amiodarone to multiple organs must be monitored. Prompt cessation of the drug should be considered upon diagnosis.

【 授权许可】

CC BY