Abstract

Amiodarone is a benzofuran derivative with a chemical structure similar to thyroxine. Originally introduced to treat angina pectoris, amiodarone was found to have antiarrhythmic properties, and in 1985, was approved in the United States for treatment of life-threatening ventricular arrhythmias. It is now used for various ventricular and supraventricular arrhythmias refractory to conventional first-line medications, and as a result, side effects have been observed with increased frequency. The most severe and potentially life-threatening of these side effects is the development of pulmonary toxicity. Typically, amiodarone pulmonary toxicity (APT) is manifested by acute pneumonitis and chronic fibrosis. Amiodarone-associated hemoptysis (AAH) is a rare occurrence. The authors describe a case of AAH successfully treated with cessation of drug and steroid therapy.

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