Amiodarone, an iodinated benzofuranic derivative, is often used in the treatment of cardiac arrhythmias. A number of side effects have been reported in up to 74% of patients at 1 year, including pulmonary fibrosis, thyroid disease, corneal deposits and neurologic disorders. Transient asymptomatic elevation of transaminases can occur in ∼25% of patients on chronic oral therapy, however acute hepatitis, severe cholestasis and cirrhosis are rarely documented. We present a case of acute fulminant hepatic failure following initiation of amiodarone with rapid resolution on its discontinuation. The patient is a 67year old gentleman with a past medical history significant for coronary artery disease and end stage renal disease on hemodialysis. He initially presented to an outside facility with a ventricular arrhythmia that required defibrillator placement and intravenous loading of amiodarone followed by oral therapy. Shortly after discharge, the patient developed increasing confusion and profound weakness and was readmitted. On this hospitalization, he was noted to have a profound hypoglycemia with a dramatic elevation in aminotransferases, as well as total bilirubin, alkaline phosphatase and prothrombin time (ast 999, alt 1375, alkaline phosphatase 191, total bilirubin 6.8). With increasing lethargy and confusion, the patient was transferred to the intensive care unit for closer monitoring. A CAT scan of the head was unrevealing, toxicology screen and acetaminophen level negative, acute viral hepatitis panel negative. Further questioning of the patient's family did not indicate any history of heavy alcohol consumption nor the use of any herbals or other potential hepatotoxins. Amiodarone was promptly discontinued and the patient was empirically treated with n-acetylcysteine and lactulose. Over the next 5 days, the patient's liver function panel and synthetic function improved considerably with notable clearing of the patient's mentation. He was subsequently discharged to a skilled nursing facility, with almost normalization of liver tests. The absence of other causes of liver disease and the clinical course suggest that amiodarone was responsible for the development of acute hepatitis in this patient. The exact mechanism of amiodarone-related toxicity remains unknown.