INTRODUCTION:Acute liver failure is characterized by a biochemical diagnosis of liver damage along with coagulopathy defined by international normalized ratio (INR) >2.0 despite intravenous vitamin K replacement or INR >1.5 with encephalopathy, without any chronic liver disease. It is a rare occurrence in a previously healthy adolescent. We report the case of acute severe hepatitis culminating into acute liver failure with suspected Wilson disease (WD).CASE DESCRIPTION/METHODS:A 14-year-old Asian female presented with hematemesis, watery stools and abdominal pain in the right upper quadrant for two days. The patient had 2-3 episodes of vomiting consisting of semi-digested food particles, watery in consistency that gradually progressed to one episode of emesis containing bright-red blood, about 15-20 ml in quantity associated with six episodes of watery stools, without any blood or mucus. She had consumed food cooked outside a few days prior. On admission, she had a pulse of 70 beats/minute, and blood pressure of 98/50 mm Hg. Physical examination revealed icterus, tenderness in the right hypochondriac region and palpable liver, about 3 cm below the costal margin. Laboratory investigations revealed hemoglobin of 10.7 gm/dl, aspartate aminotransferase of 9018 U/L, alanine aminotransferase of 6637 U/L, alkaline phosphatase of 261 U/L, total bilirubin of 2.8 mg/dl with a direct component of 1.6 mg/dl, prothrombin time of 32 seconds, partial thromboplastin time of 39 seconds, international normalized ratio of 2.69. Workup for viral markers was negative. Ultrasound of the abdomen revealed altered echotexture of the liver. The ophthalmologic examination did not reveal any abnormality. The serum ceruloplasmin level was 13 mg/dL. The patient was diagnosed with acute severe hepatitis with acute liver failure with suspected underlying WD. She was treated with intravenous doses of antibiotics including ciprofloxacin and amikacin, vitamin K, and octreotide, oral lactulose and ursodeoxycholic acid and was transfused two units of fresh frozen plasma. A gradual decrease of liver enzymes (Figure 1) and coagulation profile (Figure 2) was seen and she was followed up on an outpatient basis.DISCUSSION:The management of acute liver failure can be arduous requiring early diagnosis and aggressive treatment to improve better prognosis. Physicians should maintain a high amount of suspicion of concomitant disease in the setting of a young patient such as ours presenting with fulminant liver disease.