Finds drug-induced autoimmune-like hepatitis linked to turmeric use, indicating immune sensitization.
Drug-induced autoimmune-like hepatitis (DI-ALH) is a rare form of drug-induced liver injury (DILI) that mimics autoimmune hepatitis (AIH). Commonly implicated agents include minocycline, nitrofurantoin, and infliximab, though a wide range of other drugs has been reported. We report a 65-year-old woman with a history of suspected turmeric-induced liver injury six years prior who presented with nausea and painless jaundice two weeks after restarting the same turmeric supplement containing black pepper extract. She denied alcohol or hepatotoxic medication use, and family and personal history of autoimmune or liver disease were unremarkable. Laboratory evaluation revealed marked transaminase elevation (AST 4310 U/L, ALT >2500 U/L), total bilirubin 18.3 mg/dL, and INR 1.1. Autoimmune testing revealed positive smooth muscle antibodies and elevated IgG, while viral, metabolic, and genetic studies were negative. Imaging demonstrated periportal edema. Despite supplement discontinuation, liver enzymes worsened, prompting a liver biopsy, which demonstrated acute hepatitis with portal and lobular inflammation, plasma cell predominance, and canalicular cholestasis without fibrosis consistent with DI-ALH. Corticosteroid therapy led to biochemical improvement over three weeks. The temporal association with exposure, autoimmune serologies, characteristic histology, and steroid responsiveness supported the diagnosis of recurrent turmeric-induced DI-ALH, with more severe injury on re-exposure suggesting immune sensitization. Piperine, included to enhance curcumin bioavailability, may potentiate hepatotoxicity. DI-ALH should be considered in patients with liver injury and recent supplement use, as immunosuppressive therapy may be beneficial when injury persists after drug withdrawal.
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Patel et al. (2026) studied this question.
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