P3910 - Should We Start Treating Intravenous Amiodarone-Induced Liver Injury with N-Acetylcysteine? A Successful Treatment Case Report

Prava Karki, MD¹, Joanna Lenik, MD², Niyati Gupta, MD³, Ahmed Shady, MD^1
1Metropolitan Hospital Center, New York, NY; ²NYC Health + Hospitals/Metropolitan Hospital, Manhattan, NY; ³NYCHH/Metropolitan Hospital, New York, NY

Introduction: Amiodarone is a potent anti-arrhythmic drug used to treat atrial fibrillation. Acute hepatotoxicity is a rare but potentially fatal complication of intravenous Amiodarone. We present a case of Amiodarone induced liver injury that improved after discontinuation and treatment with N-acetyl cysteine (NAC

Case Description/Methods: A 74-year-old woman with a past medical history of seizure and atrial fibrillation was admitted for a witnessed seizure. Vital signs were normal except for tachycardia of 140. Electrocardiogram showed atrial fibrillation with a rapid ventricular rate. She was treated with a bolus of amiodarone followed by a continuous amiodarone infusion. Initial laboratory data included an alanine aminotransferase (ALT) of 44 U/L, aspartate aminotransferase (AST) 132 U/ L and creatinine kinase (CK) 2,365 U/L compared to normal values three months prior. Twelve hours later, her aminotransferases had risen further (AST 3,150 U/L, ALT 784 U/L) and her international normalized ratio (INR) was 1.6. Serial hepatic function tests showed worsening liver function with AST up to 9192 U/L, ALT 2200 U/L and INR 6.0. Gamma-GT and alkaline phosphatase were normal. Abdominal ultrasonography, viral hepatitis serology (hepatitis A, B, C, E, cytomegalovirus, Epstein-Barr, HIV, parvovirus, HSV), metabolic panels (ferritin, ceruloplasmin, alpha-1 antitrypsin) and autoimmune markers (antinuclear antibody, anti-smooth muscle antibody, anti-liver/kidney microsomal antibody) were unremarkable. Elevated INR favored high suspicion for amiodarone-induced liver injury over rhabdomyolysis induced elevated transaminase and was discontinued after about 20 hours after its first administration and she was started on a NAC protocol with subsequent improvement in her liver enzymes.

Discussion: This case illustrates the potential for amiodarone to cause acute hepatotoxicity. While the mechanism is uncertain, several have been proposed including an immunologically mediated mechanism, a free radical-based mechanism involving peroxidative injury to membrane lipids and necrosis, and a mechanism based on increased expression of the PPAR-α gene secondary to disrupted hepatic lipid mechanism. Aside from discontinuation of amiodarone, treatment is mainly supportive. While the role of NAC in non-acetaminophen induced liver injury has not been extensively studied, given its safety profile and potential for ameliorating amiodarone- induced liver injury its use may be warranted.


Disclosures:


Prava Karki, MD¹, Joanna Lenik, MD², Niyati Gupta, MD³, Ahmed Shady, MD¹. P3910 - Should We Start Treating Intravenous Amiodarone-Induced Liver Injury with N-Acetylcysteine? A Successful Treatment Case Report, ACG 2023 Annual Scientific Meeting Abstracts. Vancouver, BC, Canada: American College of Gastroenterology.