SummaryWhat is known and objective
Amiodarone, a commonly used class III antiarrhythmic agent notable for a relatively long half-life of up to 6 months and its pronounced adverse effect profile, is used for both acute and chronic management of cardiac arrhythmias. Chronic use of amiodarone has been associated with asymptomatic hepatotoxicity; however, acute toxicity is thought to be uncommon. There are only six reported cases of acute liver failure (ALF) secondary to amiodarone. In all these cases the outcome of death during the same hospitalization resulted. We aimed to report the only case of acute liver failure secondary to amiodarone infusion in the existing literature where the patient survived.

Case summary
A 79-year-old woman admitted with atrial flutter was being treated with intravenous (IV) amiodarone when she abruptly developed coagulopathy, altered mental status and liver enzyme derangement. She was diagnosed with acute liver failure (ALF) secondary to an amiodarone adverse drug reaction, with a calculated score of seven on the Naranjo adverse drug reaction probability scale. Amiodarone was immediately withheld, and N-acetylcysteine (NAC) was initiated. Clinical improvement was seen within 48 hours of holding the drug and within 24 hours of initiating NAC. On post-hospital follow-up visit she was reported to have complete recovery.

What is new and conclusion
This report emphasizes the importance of monitoring liver enzymes and mental status while a patient is being administered IV amiodarone. N-acetylcysteine administration may have possibly contributed to the early and successful recovery from ALF in our patient. To date, she is the only patient in the existing literature who has been reported to survive ALF secondary to amiodarone administration.

Acute liver failure with amiodarone infusion: A case report and systematic review

Amiodarone is believed to have caused acute hepatitis 24 hours after intravenous administration in two patients in whom no other alternative cause of hepatitis was found.

Acute Hepatitis After Parenteral Amiodarone Administration

Radiomics help move cross-sectional imaging into the domain of quantitative imaging to assess the lesions, their stoma as well as in their temporal monitoring We applied and assessed the accuracy of radiomics for differentiating healthy liver from diffuse liver diseases (cirrhosis, steatosis, amiodarone deposition, and iron overload) on non-contrast abdomen CT images in an institutional-reviewed board-approved, retrospective study Our study included 300 adult patients (mean age 63 ± 16 years; 171 men, 129 women) who underwent non-contrast abdomen CT and had either a healthy liver (n = 100 patients) or an evidence of diffuse liver disease (n = 200) The diffuse liver diseases included steatosis (n = 50), cirrhosis (n = 50), hyperdense liver due to amiodarone deposition (n = 50), or iron overload (n = 50) We manually segmented the liver in one section at the level of the porta hepatis (all 300 patients) and then over the entire liver volume (50 patients) Radiomics were estimated for the liver, and statistical comparison was performed with multiple logistic regression and random forest classifier With random forest classifier, the AUC for radiomics ranged between 072 (iron overload vs healthy liver) and 098 (hepatic steatosis vs healthy liver) for differentiating diffuse liver disease from the healthy liver Combined root mean square and gray-level co-occurrence matrix had the highest AUC (AUC:099, p < 001) for differentiating healthy liver from steatosis Radiomics were more accurate for differentiating healthy liver from amiodarone (AUC:093) than from iron overload (AUC:079) Radiomics enable differentiation of healthy liver from hepatic steatosis, cirrhosis, amiodarone deposition, and iron overload from a single section of non-contrast abdominal CT The high accuracy of radiomics coupled with rapid segmentation of the region of interest, radiomics estimation, and statistical analyses within the same prototype makes a compelling case for bringing radiomics to clinical use for improving reporting in evaluation of healthy liver and diffuse liver diseases

Accuracy of radiomics for differentiating diffuse liver diseases on non-contrast CT.

The case is reported of a 39-year-old severely obese woman who developed acute metabolic disorders after the administration of a short course of intravenous amiodarone. The main biological features were hypertriglyceridemia, hypoglycaemia, hyperlactatemia and hyperammonemia; all were reversible after amiodarone discontinuation. There was an associated rise in liver enzymes. However, the influence of co-factors on these metabolic disorders, such as acquired carnitine deficiency, severe obesity, a long-term course of pancreatitis, and abdominal infections, could not be excluded.

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Hyperammonemic Encephalopathy and Lipid Dysmetabolism in a Critically Ill Patient After a Short Course of Amiodarone

A 74-year-old man with heart failure and atrium fibrillation was admitted to hospital in case of persistent dyspepsia and disturbed liver test functions. Ultrasound and detailed laboratory tests didn’t reveal infectious disease of the liver or biliary obstruction. A diagnosis of hepatotoxicity due to amiodarone use was made. Withdrawal of the drug led to complete recovery of symptoms and normalization of laboratory tests.

A Late Presentation of Amiodarone -Induced Hepatotoxicity

Objectives Amiodarone is a commonly used antiarrhythmic drug. Hepatotoxicity following chronic oral administration occurs in 1% to 3% of patients. Hepatotoxicity following intravenous (IV) administration is infrequent but may be associated with dramatic increases in serum transaminases. We describe the incidence of liver toxicity among patients receiving IV amiodarone during a 5-year period. Methods This was a single-center retrospective review of patients receiving IV amiodarone for any cause. The outcome measures were development of elevated serum transaminases and the relation of transaminitis to all-cause 30-day mortality. Results A total of 1510 patients received amiodarone intravenously between 2005 and 2011; 77 (5%) developed elevated liver enzymes. Enzyme elevation was divided into mild (100-300 IU/L), moderate (300-1000 IU/L), and severe (>1000 IU/L). The median alanine aminotransferase was 189 (37-10,006) IU/L and aspartate aminotransferase was 253 (84-12,005) IU/L. The 30-day mortality among those with transaminitis was 22%; however, no patient died of amiodarone-related liver disease. Conclusions Amiodarone can cause severe elevation in liver enzymes. The incidence of severe transaminitis is low; deaths following IV amiodarone are rarely caused by drug-induced liver failure.

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Sharon Kim

Papers

Hepatic Dysfunction in Patients Receiving Intravenous Amiodarone