Amiodarone is a potent antiarrhythmic agent.
Liver injury
Amiodarone causes elevated liver enzymes in up to 30% of patients and steatohepatitis in 1–2% of patients.
The majority of cases display liver enzyme abnormalities within 24 h of intravenous infusion.
Even low oral dosing (200 mg daily) may trigger steatohepatitis with cumulative use.
Occasionally, jaundice is the major clinical presentation. These cases often show hepatocellular necrosis and fibrosis, and have a poor prognosis.
Amiodarone steatohepatitis is characterised by prominent Mallory hyaline (occasionally in zone 1) and neutrophilic satellitosis, while steatosis is less conspicuous.
The findings can be similar to alcoholic steatohepatitis. Reversal of liver injury often occurs with discontinuation of the drug but may be delayed by weeks or months.
In addition, amiodarone is also associated with a different type of lipid accumulation called "phospholipidosis" characterised by accumulation of drug in the lysosomes.
This leads to "foamy" appearance of hepatocytes and Kupffer cells. The foamy areas show lamellar lysosomal inclusion bodies on electron microscopy.
Phospholipidosis is not always seen in amiodarone toxicity and is independent of steatohepatitis.
See also
drug-induced steatohepatitis
References
Lewis JH, Mullick F, Ishak KG, Ranard RC, Ragsdale B, Perse RM, Rusnock EJ, Wolke A, Benjamin SB, Seeff LB, et al. Histopathologic analysis of suspected amiodarone hepatotoxicity. Hum Pathol. 1990 Jan;21(1):59-67. PMID: 2403975