OasisLMS

Drug-induced liver injury (DILI) is a major cause of acute liver failure, yet its onset is highly unpredictable and not fully explained by established clinical risk factors. Known HLA allele associations, such as HLA-B*57:01, HLA-A*33:01, and HLA-DRB1*15:01 implicated in DILI due to flucloxacillin, amoxicillin-clavulanate, terbinafine, and other drugs, represent an essential component of the complex genetic architecture underlying DILI. However, the low positive predictive value constrains their clinical implementation. Even with limited case numbers due to the rarity of the clinical phenotype, recent genome-wide association studies (GWAS) suggest that DILI risk is influenced by the combined effects of HLA risk alleles and other common variants, mostly implicated in immune function, but each with a small effect size. Consequently, polygenic approaches are emerging as a promising strategy for estimating an individual’s inherited risk of drug-specific liver injury.

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