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Oral iron chelation with deferasirox is widely used to manage iron overload in patients with thalassemia syndromes. Clinically significant drug-induced liver injury (DILI) attributed to deferasirox is uncommon but has been reported. We describe a 49-year-old man with non-transfusion-dependent β-thalassemia intermedia (β-thalassemia trait with α-globin gene triplication), substantial iron overload, cirrhosis, and previously treated hepatocellular carcinoma who developed acute hepatic decompensation during deferasirox therapy. He presented with progressive jaundice, ascites, and encephalopathy. Laboratory evaluation showed profound conjugated hyperbilirubinemia with relatively modest aminotransferase elevations, consistent with a predominantly cholestatic pattern of injury. Causality assessment using the Roussel Uclaf Causality Assessment Method (RUCAM) yielded a score of 7, indicating a probable association with deferasirox. Despite drug withdrawal and supportive care, including plasma exchange, liver failure persisted, and the patient was evaluated for urgent transplantation. This case underscores the vulnerability of patients with limited hepatic reserve to chelator-associated hepatotoxicity and highlights the need for individualized chelation strategies and close biochemical monitoring.
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Wimalasiri et al. (2026) studied this question.
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