ArticleLiver international : official journal of the International Association for the Study of the Liver2024
Drug-induced liver injury (DILI) ascribed to non-steroidal anti-inflammatory drugs (NSAIDs) in the USA-Update with genetic correlations.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The incidence of chronic drug-induced liver injury: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Leveraging Administrative Health Data to Capture Rare Adverse Drug Reactions: Identifying Pediatric Patients With Trimethoprim-Sulfamethoxazole Acute Respiratory Distress Syndrome.Pharmacology research & perspectives · 2026Article
- Genetic Variants Associated with Non-Steroidal Anti-Inflammatory Drug-Induced Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis.Medical sciences (Basel, Switzerland) · 2026Article
- Human Leukocyte Antigen (International journal of molecular sciences · 2026Review
- Genetic and Genomic Approaches to the Study of Drug-Induced Liver Injury.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- The clinical application of genetic testing in DILI, are we there yet?Clinical liver diseaseReview
Corrections and comments
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Authors and funding
12 authors at 10 institutions in 2 countries.
Funding
Abstract
objectiveTo describe patients with NSAID-DILI, including genetic factors associated with idiosyncratic DILI.
methodsIn DILIN, subjects with presumed DILI are enrolled and followed for at least 6 months. Causality is adjudicated by a Delphic approach. HLA sequencing of multiethnic NSAID-DILI patients and HLA allele imputation of matching population controls were performed following overall, class and drug-based association analysis. Significant results were tested in a non-Hispanic White (NHW) case-control replication cohort.
resultsBetween September 2004 and March 2022, causality was adjudicated in 2498, and 55 (41 [75%] women) were assessed as likely due to NSAIDs. Median age at onset was 55 y (range 22-83 y). Diclofenac was the causative drug in 29, celecoxib in 7, ibuprofen in 5, etodolac and meloxicam each in 4. Except for meloxicam and oxaprozin (n = 2), the liver injury was hepatocellular with median R 15-25. HLA-DRB1*04:03 and HLA-B*35:03 were significantly more frequent in NSAID-DILI patients than in non-NSAID DILI controls. Interestingly, 85% of the HLA-DRB1*04:03 carriers developed DILI due to the use of acetic acid derivative NSAIDs, supporting the hypothesis that HLA-DRB1*04:03 could be a drug and/or class risk factor. HLA-B*35:03 but not HLA-DRB1*04:03 association was confirmed in the independent NHW replication cohort, which was largely driven by diclofenac.
conclusionsDespite prevalent use, NSAID-DILI is infrequent in the United States. Diclofenac is the most commonly implicated, and adherence to warnings of risk and close observation are recommended. The increased frequency of HLA-B*35:03 and DRB1*04:03, driven by diclofenac, suggests the importance of immune-mediated responses.
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