Cholestatic Liver Injury following Re-initiation of Carbimazole in a Patient with Graves’ Disease: A Case Report

Carbimazole is a commonly used Antithyroid Drug (ATD) for the treatment of Graves’ Disease (GD). Although generally well tolerated, it can rarely cause drug-induced liver injury, typically presenting with a cholestatic pattern. Carbimazole-induced cholestatic liver injury is an uncommon and often underrecognised complication that may pose a diagnostic challenge. In this case, a 46-year-old man presented with jaundice for one month, along with pruritus, nausea, anorexia, weight loss, palpitations, heat intolerance, and tremors. He had GD and had been off treatment for nearly one year before restarting carbimazole 10 mg twice daily two months before presentation. The patients had symptoms of hyperthyroidism and jaundice. Laboratory tests showed conjugated hyperbilirubinaemia with a cholestatic pattern of liver injury and preserved liver synthetic function. Thyroid function tests confirmed thyrotoxicosis, and positive thyroid autoantibodies were consistent with GD as the underlying aetiology. Viral markers and autoimmune liver tests were negative. Imaging ruled out biliary obstruction, and liver biopsy showed cholestatic injury with canalicular bile plugs, consistent with carbimazole-induced cholestatic liver injury. Carbimazole was stopped, and two cycles of low-volume plasma exchange were performed. Thyrotoxicosis was controlled with Lugol’s iodine, dexamethasone, and propranolol, followed by total thyroidectomy. This case highlights that even late presentation and toxicity following re-initiation of carbimazole should be considered in patients presenting with cholestatic liver injury.