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
The evidence is unambiguous: glutathione's antioxidant function depends entirely on the reduced thiol group remaining intact, and every hour above 8C or past the 28-day mark increases the probability that group has oxidised
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Insulin resistance drives both type 2 diabetes and cardiovascular disease through overlapping mechanisms
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Although glucagon is traditionally understood as a counter-regulatory hormone that increases hepatic glucose production, its pharmacologic activation in balanced multi-receptor agonists may contribute to weight reduction by increasing energy expenditure, promoting fatty acid oxidation, and improving hepatic lipid metabolism
