Propafenone Hepatotoxicity: Report of a New Case and Review of the Literature
A 67-year-old female patient presented to the emergency department of the American University of Beirut Medical Center because of the progressive appearance of painless jaundice of two weeks duration.\nThe patient's past medical history was noted for left breast cancer (in remission). She denied alcohol intake or illicit drug abuse.\nSix weeks prior to the onset of jaundice, she had presented with high-rate atrial fibrillation and was commenced on propafenone at 300 mg/day.\nUpon presentation, she was icteric. The physical examination revealed minimal nontender hepatomegaly.\nA computed tomography scan performed at another facility showed prominent common bile and pancreatic ducts suggesting a double duct sign. Her initial serum bilirubin was 9.4/7.7 mg/dL, alkaline phosphatase of 384 IU/L. Her alanine transferase was 213 IU/L and aspartate transferase 228 IU/L. Her CA19-9 was 70 IU/mL []. Endoscopic ultrasound done at our center showed normal common bile and pancreatic ducts and no ampullary or pancreatic masses. Subsequently, viral serologic markers (IgM hepatitis A virus, IgM Hepatitis B core, Hepatitis C virus antibodies, Epstein-Barr virus, Cytomegalovirus) were negative. The anti-nuclear, anti-smooth muscle, anti-mitochondrial, and anti-liver and anti-kidney microsome antibodies’ levels were within normal limits. A Magnetic resonance cholangiopancreatography suggested a left hepatic stricture, but Endoscopic retrograde cholangiopancreatography was normal.\nA liver biopsy via a trucut needle showed active portal and periportal inflammation with moderate macrovesicular steatosis, and bile ductular proliferation [Figure and ].\nWithdrawal of propafenone was associated with gradual decrease in serum alkaline phosphatase and gamma-glutamyl transferase along with normalization of the aminotransferase levels and CA19-9.