INTRODUCTION: Propafenone, an antiarrhythmic medication, decreases cardiac automaticity and increases refractory periods slowing cardiac conduction. Propafenone-induced hepatic injury is rare with only eight reported cases in the literature. We report a case of propafenone-induced hepatic injury in a patient presenting with painless jaundice. CASE DESCRIPTION/METHODS: A 60-year-old woman presented with sudden onset jaundice and a one week history of 10-pound weight loss, right upper quadrant abdominal pain, nausea and vomiting. Two months prior to presentation, she was diagnosed with atrial fibrillation and was begun on Propafenone 325 mg oral twice daily. She had no history of alcohol, drugs, or herbal medication use. Physical exam was significant only for generalized jaundice. On admission, laboratory studies were significant for AST 304 IU/L, ALT 601 IU/L, ALP 334 IU/L, total bilirubin 7.9 mg/dL, and direct bilirubin 5.4 mg/dL.Abdominal ultrasound revealed fatty liver without biliary obstruction. CT abdomen was unremarkable for hepatic or biliary pathology. Viral serologic markers and acetaminophen levels were negative as well as workup for Autoimmune hepatitis, and Primary biliary cholangitis. Liver biopsy revealed steatohepatitis with superimposed ductular and centrilobular cholestasis suggestive of drug-induced injury.The patient was begun on N-Acetylcysteine and Propafenone was discontinued. Several days after withdrawal of Propafenone, liver function tests began to improve slowly. The patient was discharged home and one month later, transaminases returned to normal and jaundice had resolved. DISCUSSION: Propafenone is a Class 1C antiarrhythmic indicated for symptomatic atrial fibrillation without structural abnormalities. The mechanism for hepatic injury is unknown. Like in our patient, the injury is self-limited and has not been linked to acute liver failure, chronic liver injury, or vanishing bile duct syndrome. Once identified as the cause, the medication should be immediately stopped and never prescribed because re-exposure is associated with recurrence of symptoms. As in other reports, our patient’s liver injury occurred within a 2-6-week period after exposure and, resolved 3-5 weeks after cessation of the offending medication. Propafenone-induced hepatic injury should be suspected in a patient presenting with hepatocellular and cholestatic injury, especially in a patient recently begun on that medication after exclusion of other causes of abnormal liver function.
INTRODUCTION: Duplicated gallbladder (DG) is a rare congenital anomaly, affecting approximately 1 in 4000 births. Few reports exist describing acute cholecystitis in DG patients, with even less case reports of chronic cholecystitis. In this case we present a case of CC in a Hispanic woman with a DG. CASE DESCRIPTION/METHODS: A 49-year-old Hispanic woman with a history of dyslipidemia and diabetes presents to the ED with a 5-hour history of 10/10 crampy, mid-epigastric, non-radiating abdominal pain associated with subjective fevers, nausea and non-bloody, non-bilious vomiting. Patient had similar pain episodes in the past requiring hospital admissions. She was hemodynamically stable with a physical exam remarkable for moderate distress from pain and significant epigastric and right lower quadrant abdominal tenderness on palpation. Laboratory exam was significant for WBC- 12 th/uL (N: 4.8-10.9 th/uL), hemoglobin - 9.0 gm/dL (10.8-14.7 gm/dl) and ALP- 133 IU/L (N: 34-104 IU/L). Urinalysis was positive for WBC, bacteria, leukocyte esterase and nitrite. Abdominal ultrasound, CT abdomen and HIDA scan were suggestive of a DG. The patient was taken for a cholecystectomy. In the OR she was found to have a DG with 2 fundi merged at the Hartman's pouch, likened to the Boyden's vesica fellea divisa classification type. Pathology results revealed chronic cholecystitis and cholesterolosis in the DG. Patient continues to maintain significant clinical improvement post-surgery and she continues to be under close follow-up. DISCUSSION: CC is defined by the histopathologic appearance of chronic inflammation of the gallbladder and is believed to develop due to the presence of gallstones, although cases of acalulous CC also exist. As in our case, patients typically present with pain, however pain severity and liver enzyme alterations do not usually correlate with disease presence. To the best of our knowledge, no similar cases have been reported in the Hispanic population. In patients presenting to the ER, a high index of suspicion is recommended to improve overall patients' outcomes especially in patients presenting with multiple disease processes.
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