INTRODUCTION

Pemoline is a central nervous system stimulant that increases dopamine and norepinephrine at the synaptic cleft. It is an alternative to methylphenidate in treating attention deficit hyperactivity disorder (ADHD). The mechanism of pemoline-induced hepatic injury is unclear although immunologically mediated hypersensitivity and dose-dependent hepatotoxicity reactions have been postulated.^1-7 We describe a patient who, after pemoline administration, developed acute hepatic failure with features of autoimmune hepatitis.

	CASE REPORT

A 7-year-old boy with Duchenne muscular dystrophy (DMD) and ADHD presented for evaluation of fever, vomiting, and jaundice. He was previously well (Table). His initial evaluation was remarkable for an alanine aminotransferase of 2316 U/L, (0-35) an aspartate aminotransferase of 467 U/L, (0-35) a total bilirubin of 111 µmol/L, (2-18) and a direct bilirubin of 74 µmol/L (0-8) as well as negative anti-hepatitis A virus (immunoglobulin M and total), hepatitis B surface antigen, hepatitis B surface antibody, and hepatitis B core antibody (immunoglobulin M and total). The only medications he had received were pemoline (56.25 mg/day) and cyproheptadine (2 mg/day); the latter medication was prescribed after the patient's appetite decreased while on pemoline. Pemoline was discontinued after 8 months of usage as the presumed etiology of his elevated aminotransferases. Two weeks later, he developed altered mental status and persistent jaundice. He was transferred to Children's Hospital Medical Center.

Table Removed (Available Only in the Full Text)

His family history was remarkable for eight male relatives with DMD. There was no family history of autoimmune disorders or liver disease. On physical examination, he was thin and afebrile. His weight was 18 kg (<5th%). His . . . [Full Text of this Article]