Table 1

Classification of DILI based on liver enzyme derangement1

PhenotypeCase definitionCommonly implicated agents
 IdiosyncraticHepatocellular: If ALT alone is elevated less than fivefold above ULN or R≥5.
Cholestatic: ALP alone is elevated less than twofold above ULN or R≤2.
Mixed: R>2 to<5
Chronic DILI: DILI with acute presentation, with evidence of persistent liver injury at >1 year after its onset
Antimicrobials, anticonvulsants, antiarrhythmic, androgens, oestrogens/progesterone, immunomodulatory and antineoplastic
Drug reaction with eosinophilia and systemic symptomsDrug-related hypersensitivity with eosinophilia and systemic inflammationAnticonvulsants, NRTIs
Drug-induced autoimmune hepatitisAcute DILI with serological and/or histological features of AIHNSAIDs, statins, minocycline and nitrofurantoin
Secondary sclerosing cholangitisPresenting as acute DILI with histological/radiological features of sclerosing cholangiopathyInhalational anaesthetics, atorvastatin, 6-MP
Granulomatous hepatitisGranulomas on histology with exposure to implicated agent(s)Anticonvulsants, sulphonamides
Acute fatty liverAcute development of microvesicular steatohepatitisReverse transcriptase inhibitors
Drug-associated fatty liver diseaseConsistent with NAFLD and attributable exposureMethotrexate, corticosteroids, 5-FU
Nodular regenerative hyperplasiaDiffuse nodularity organised around central hepatocytesAntineoplastic/cytotoxic
DuctopaeniaChronic cholestasis and ductular lossAntimicrobials (β-lactams, tetracyclines and sulphonamides)
Liver tumoursFeatures of hepatocellular adenoma or carcinoma dependent of histological/imaging characteristicsAnabolic androgenic steroids and oral contraceptives
  • 5-FU, 5-fluorouracil; 6-MP, 6-mercaptopurine; AIH, autoimmune hepatitis; ALP, alkaline phosphatase; ALT, alanine transferase; DILI, drug-induced liver injury; NAFLD, non-alcoholic fatty liver disease; NRTI, nucleoside reverse transcriptase inhibitor; NSAID, non-steroidal antiinflammatory drug; ULN, upper limit of normal.