A fifteen-year-old girl was treated with
isoniazid (INH) for
latent tuberculosis infection (LTBI), and subsequently developed epigastric
pain,
vomiting, and
jaundice after three months of treatment. Acute
fulminant hepatic failure was diagnosed. INH was stopped, and she received N-acetyl
cysteine and
Vitamin K. Liver biopsy showed moderate to severe lymphocytic and plasmacytic portal and lobular
inflammation, prominent ductal proliferation, moderate
cholestasis (predominantly hepatocellular and canalicular), hepatocellular damage, and stage 3 bridging
fibrosis. She was treated with
steroids and
azathioprine for probable
autoimmune hepatitis (AIH). She received six months of
rifampicin treatment for LTBI. Liver biopsy two years later showed mild portal
inflammation, predominantly lymphocytitic, mild portal
fibrosis without bridging, irregular bile ducts without
cholestasis, and no significant hepatocellular damage; overall the later biopsy demonstrated significant improvement. This case illustrates overlapping morphologic presentation in INH hepatotoxicity with hepatocellular injury and plasma cell infiltrate (due to probable AIH), as well as cholestatic features. Although her follow-up liver biopsy indicated lymphocytic
inflammation, she is now asymptomatic with normal hepatic
transaminases.