2217 Silent Propafenone-Induced Liver Injury: Case Report

Abstract

INTRODUCTION: Propafenone is a class Ic antiarrhythmic. It is metabolized primarily by hepatic cytochrome P-450 2D6 and rarely associated with liver toxicity. We report a case of silent propafenone-induced liver injury. CASE DESCRIPTION/METHODS: An 82-year-old man with DM, HTN, COPD, moderate mitral valve regurgitation, CABG, and aortic valve replacement, presented with progressive SOB and orthopnea of 2-week duration. Two weeks prior, he had atrial fibrillation treated with ablation, apixaban, and propafenone. Other medications were losartan, amlodipine, and furosemide. He denied alcohol/illicit drug use. He was alert, oriented, in moderate respiratory distress, and non-icteric. Temperature was 37.4 C, BP 155/67, HR 112, and RR 18. He had shallow breath sounds with bilateral diffuse crackles, bilateral lower extremity pitting edema, and unremarkable abdominal exam. EKG showed atrial fibrillation. He was treated with IV diltiazem and furosemide with improvement of SOB. However, on routine investigations, AST was 2182 IU/L, ALT 1805 IU/L, alkaline phosphatase 210 IU/L, total/direct bilirubin 4.6/1.0 mg/dL, and INR 3.4. Urine and serum toxicology, IgM hepatitis A virus, IgM hepatitis B core, hepatitis B surface antigen, hepatitis C virus Ab, Epstein-Barr virus, and cytomegalovirus were negative. ANA, smooth muscle Ab, LKM Ab, celiac serology, ceruloplasmin, alpha 1 antitrypsin, iron studies, and acetaminophen levels were all normal. Ultrasounography showed normal common bile duct and no intrahepatic biliary dilatation and was consistent with hepatocellular disease. Hepatic vessels doppler was unremarkable. Propafenone was discontinued and 5 days later, AST was 148, ALT 581, alkaline phosphatase 132, total/direct bilirubin 1.1/0.5; all tests normalized within 2 weeks. DISCUSSION: Hepatotoxicity secondary to propafenone is rare; only 9 cases have been previously reported. Our patient developed hepatotoxicity 2 weeks after starting propafenone, had immediate improvement after its withdrawal, and work up was otherwise negative, strongly suggesting propafenone as the cause. Similar to previous cases, hepatotoxicity had a cholestatic pattern and was completely reversible. Unlike previous cases where jaundice, pruritis, and abdominal pain were presenting symptoms; hepatotoxicity was incidentally discovered in our patient. Although very rare, clinicians should be aware of propafenone-associated hepatotoxicity and routine monitoring of hepatic function may be warranted.