Gene-guided N-acetyl Cysteine for Prophylaxis of Anti-tuberculous Drug- Induced Hepatitis

Tuberculosis (TB) remains a significant public health concern in Thailand and globally, especially in tropical regions, with pulmonary TB being predominant. Besides affecting the lungs, TB can also impact extrapulmonary organs. Standard TB treatment involves a combination of drugs administered for at least 6 months, but it can cause adverse effects such as hepatitis. Hepatotoxicity, occurring in 20-60% of patients, is commonly linked to isoniazid, rifampicin, and pyrazinamide. Slow acetylators of the NAT2 gene are particularly susceptible. Previous research suggests N-acetylcysteine (NAC) may mitigate hepatotoxicity, especially among slow acetylators. A recent study by Kittichai Samaithongcharoen and team showed that NAC reduced hepatotoxicity incidence significantly among slow acetylators. This underscores the potential of NAC in preventing drug-induced hepatotoxicity in TB treatment, warranting further investigation against standard treatment protocols.

NCT Number	NCT06484530
Lead Sponsor	Mahidol University
Conditions	Tuberculosis (TB), Isoniazid Toxicity, Rifampicin Toxicity, Pyrazinamide Adverse Reaction, Ethambutol Toxicity, NAT2 Slow Acetylator Status, NAT2 Rapid Acetylator Status, NAT2 Polymorphism +1 more
Enrollment	116 participants
Start Date	2024-03-12
Primary Completion	2024-09-18 (estimated)
Study Completion	2024-09-18 (estimated)
Updated on ClinicalTrials.gov	2024-07-03