The incidence of carbimazole-induced liver injury (DILI) in patients treated for hyperthyroidism is infrequent, ranging from 0.1% to 0.5%. Whilethe injury usuallyfollows a cholestatic pattern, the condition can also present with mixed or cytolytic features, driven by either immune-mediated responses or the metabolic involvement of cytochrome P450 enzymes.We report the case of a 29-year-old woman with Graves’ disease (free T4: 78 pmol/L) who developed severe hepatotoxicity two weeks after initiating 40 mg/dayof Carbimazole. The patient presented with clinical jaundice and laboratory findings of significant cholestasis. After excluding viral, autoimmune, and structural etiologies, a diagnosis of carbimazole-induced hepatotoxicity was established. Management included immediate cessation of the antithyroid drug, initiation of corticosteroid therapy (1 mg/kg/day), and a session of plasmapheresis to bridge the patient safely toward a thyroidectomy. Liver function showed marked improvement within one week of discontinuation. These findings suggest that when conventional cessation of the drug is insufficient to stabilize rapidly deteriorating liver enzymes, advanced extracorporeal therapies may serve as a crucial bridge to definitive surgical intervention. Ultimately, this report reinforces the necessity of vigilantmonitoring of liverfunction tests during the initiation of carbimazole therapy. By advocating for proactive serial biochemical screening, we aim to standardize safer clinical practices and improve outcomes for patients requiring rapid definitive treatment in the setting of severe, unpredictable, and potentially life-threatening drug-induced liver injury caused by antithyroid medications.
Haouach et al. (Mon,) studied this question.