Isoniazid hepatotoxicity with clinical and histopathology correlate.

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.