Vol. 7, Issue 2, Part F (2025)

Background: Anti-tubercular therapy (ATT)-induced hepatotoxicity is one of the most clinically significant adverse effects of tuberculosis treatment, particularly associated with isoniazid, rifampicin, and pyrazinamide. N-acetylcysteine (NAC), a thiol-containing antioxidant and glutathione precursor, has demonstrated hepatoprotective potential beyond its established use in acetaminophen toxicity.
Case Presentation: We report the case of a 29-year-old female who developed hepatotoxicity secondary to ATT and showed marked biochemical improvement following intravenous NAC using a three-bag regimen, followed by oral maintenance therapy. Liver function tests normalized, allowing for safe reintroduction of ATT without recurrence of hepatotoxicity.
Conclusion: NAC may serve as an effective adjunct in the management of ATT-induced hepatotoxicity due to its antioxidant and mitochondrial-stabilizing effects. Further controlled trials are warranted to validate its role in drug-induced liver injury.