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