Amiodarone Induced Fulminant Hepatotoxicity: A Case Report
Published: November 1, 2018 | DOI: https://doi.org/10.7860/JCDR/2018/35445.12295
Saif Alam, Sumit Singla, Sanjay Pandit, Hermanjit Singh Hira
1. Senior Resident, Department of Medicine, MAMC and Lok Nayak Hospital, New Delhi, India.
2. Associate Proffesor, Department of Medicine, MAMC and Lok Nayak Hospital, New Delhi, India.
3. Associate Proffesor, Department of Medicine, MAMC and Lok Nayak Hospital, New Delhi, India.
4. Director Proffesor, Department of Medicine, MAMC and Lok Nayak Hospital, New Delhi, India.
Correspondence
Dr. Saif Alam,
Jawaharlal Nehru Marg, New Delhi, India.
E-mail: saifalam83@gmail.com
Amiodarone is an iodine-rich Class III antiarrhythmic drug, which acts via membrane ion channels. It is metabolised in the liver to produce the active metabolite desethylamiodarone. It is highly lipophilic with a large volume of distribution and accumulates in many different tissue, especially the liver. It is widely used in supraventricular and ventricular arrhythmias and given as a loading dose, either via the intravenous or oral route, followed by maintenance doses. The common adverse effects of amiodarone are nausea, vomiting, tremor, thyroid dysfunction, peripheral neuropathy, photosensitivity, bradyarrhythmia, worsening of arrhythmia and the less common ones are pneumonitis, optic neuropathy and hepatotoxicity.
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