Hepatic Encephalopathy Caused by Long-Term Amiodarone Use
Naoki Murata1, Toshinori Nishizawa1, Yuntae Kim2
1Department of General Internal Medicine, St. Luke's International Hospital, Tokyo, JPN.
Cureus
|January 17, 2024
Summary
Long-term amiodarone use can lead to drug-induced steatohepatitis and urea cycle abnormalities, causing hyperammonemia and hepatic encephalopathy. This case highlights the liver
Area of Science:
- Hepatology
- Cardiology
- Pharmacology
Background:
- A 72-year-old woman with hypertrophic cardiomyopathy and ventricular tachycardia was treated with amiodarone for six years.
- Amiodarone is an antiarrhythmic drug with a known potential for various toxicities.
Observation:
- The patient presented with hepatic encephalopathy after cumulative amiodarone exposure.
- Imaging revealed diffuse increased liver parenchyma attenuation, consistent with a 'bright liver' on CT.
- Liver biopsy confirmed drug-induced steatohepatitis.
Findings:
- No urea cycle genetic variations were identified.
- The patient was diagnosed with drug-induced steatohepatitis and urea cycle abnormalities secondary to amiodarone.
- Amiodarone was implicated as the cause of hyperammonemia and subsequent hepatic encephalopathy.
Implications:
- This case illustrates the potential for amiodarone to induce steatohepatitis and urea cycle dysfunction.
- Understanding this mechanism is crucial for diagnosing amiodarone-related hyperammonemia.
- Highlights the importance of considering drug toxicity in patients with unexplained liver dysfunction and encephalopathy.
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