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Glucocorticoid-mediated activation of muscle branched-chain -keto acid dehydrogenase in vivo

Skawinski M, Van Schooten FJ, Smolinska A

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Phenotype Histological features Example agents Acute fatty liver with lactic acidosis Microvesicular hepatic steatosis other tissue involvement Didanosine, Fialuridine, Valproate Acute hepatic necrosis Collapse and necrosis of liver parenchyma Isoniazid, Niacin Autoimmune-like hepatitis Plasma cells and interface hepatitis with detectable autoantibodies Nitrofurantoin, Minocycline Bland cholestasis Balloon hepatocytes with minimal inflammation Anabolic steroids Cholestatic hepatitis Balloon hepatocytes with inflammation, predominance of serum alkaline phosphate elevation (phenytoin, amoxicillin-clavulanic acid) Phenytoin, Augmentin Fibrosis/cirrhosis Hepatic collagenization with minimal inflammation Methotrexate, Amiodarone Immunoallergic hepatitis Eosinophilic infiltrate Trimethoprim-sulfamethoxazole Nodular regeneration Micro- or macroscopic liver nodules Azathioprine, Oxaliplatin, TDM1 Nonalcoholic fatty liver Macro- and microsteatosis, hepatocyte ballooning and periportal inflammation Tamoxifen Sinusoidal obstruction syndrome Inflammation with obliteration of central veins Busulfan Vanishing bile duct syndrome Paucity of interlobular bile ducts Sulfonamides, Beta-lactams Diagnosis of DILI Making a diagnosis of DILI is often very challenging due to varied presentations in varied clinical scenarios with reliable diagnostic tests

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