BACKGROUND: In some patients with Wilson disease, there can be a combined impact of active tuberculosis (TB) and anti-tuberculosis therapy (ATT), a “double hit”, due to drug-induced liver injury that can accelerate Wilson cirrhosis and result in acute liver failure. This report presents the case of a 31-year-old woman with liver cirrhosis due to Wilson disease and the combined impact of active TB and ATT resulting in acute liver injury.

CASE REPORT: A 31-year-old woman with genetically confirmed Wilson disease and Child-Pugh B liver cirrhosis presented in July 2025 with acute hepatic decompensation. Investigation revealed a positive QuantiFERON-TB Gold test result, lymphocytic exudative ascites, and a clinical picture consistent with extrapulmonary TB. Empiric ATT was initiated with rifampicin and isoniazid. Within 2 months, she re-presented with severe anti-TB drug-induced liver injury, which manifested as acute-on-chronic liver failure. The hepatotoxic regimen was immediately discontinued, and intensive supportive care was administered, resulting in gradual stabilization of liver function and clinical improvement.

CONCLUSIONS: This case demonstrates the critical “double-hit” vulnerability in Wilson disease, in which copper-mediated glutathione depletion leaves the liver unable to detoxify standard anti-TB drugs. Clinicians managing TB in patients with decompensated Wilson cirrhosis should avoid standard rifampicin-isoniazid regimens and use hepatosafe alternatives instead. A high index of suspicion for TB is warranted in all cirrhotic patients with fever, lymphocytic exudative ascites, and unexplained decompensation.

Keywords: Case Reports, drug-induced liver injury, Hepatology, Liver Cirrhosis, Tuberculosis, Wilson disease