Mortality associated with drug-induced liver injury (DILI)

Although drug-induced liver injury (DILI) is a rare clinical event, it carries significant morbidity and mortality, leaving it as the leading cause of acute liver failure in the United States. It is one of the most challenging diagnoses encountered by gastroenterologists. The development of various drug injury networks has played a vital role in expanding our knowledge regarding drug-related and herbal and dietary supplement-related liver injury. In this review, we discuss what defines liver injury, epidemiology of DILI, its biochemical and pathologic patterns, and management. (Hepatology Communications 2020;4:631-645). and Kidney Diseases established the U.S. DILI Network (DILIN) in 2003 to identify, enroll, and characterize cases of non-APAP DILI and herbal and dietary supplements (HDSs). (13) The U.S. DILIN has two registry studies at eight different academic centers across the United States. The network has expanded our understanding of DILI. Antimicrobials were noted to be the most common causative agents, accounting for 45% of cases in a 2004 study, followed by HDSs, cardiovascular drugs, central nervous system agents, antineoplastic agents, and analgesics. (14) Of the antimicrobials, amoxicillin-clavulanate (22%), isoniazid (11.7%), and nitrofurantoin (10.2%) were the top three implicated agents. (14) The network has also noted an increasing proportion of HDS-related liver injury,

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“…Similar fatality rates from DILI with hepatocellular jaundice have been seen in the Spanish DILIN (11.7%) and SADRAC (12.7%). ( 13,25,26 )…”

Section: Patterns and Outcomes Of Dilimentioning

confidence: 99%

Drug‐Induced Liver Injury in GI Practice

Sandhu

Navarro

2020

Hepatol Commun

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“…Type B ADRs, predominantly T cell-mediated drug-induced delayed hypersensitivity reactions (DHRs), presents variable severity and clinical diagnosis, from mild skin injury such as maculopapular exanthema (MPE) to life-threatening severe cutaneous adverse drug reactions (SCARs) including acute generalized exanthematous pustulosis (AGEP), drug reactions with eosinophilia and systemic symptoms (DRESS), Stevens–Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN) ( Copaescu et al, 2020 ). SCARs are rare, but they have high mortality rates (AGEP: <5%, DRESS: 5%–10%, SJS/TEN: 10%–40%) ( Bjornsson and Bjornsson, 2017 ; Oh et al, 2021 ; Huang et al, 2022 ). In global, the incidence of SCARs is reported to be 0.4–1.2 per million per years ( Verma et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Current understanding of genetic associations with delayed hypersensitivity reactions induced by antibiotics and anti-osteoporotic drugs

Wung¹,

Wang²,

Lai³

et al. 2023

Front. Pharmacol.

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Drug-induced delayed hypersensitivity reactions (DHRs) is still a clinical and healthcare burden in every country. Increasing reports of DHRs have caught our attention to explore the genetic relationship, especially life-threatening severe cutaneous adverse drug reactions (SCARs), including acute generalized exanthematous pustulosis (AGEP), drug reactions with eosinophilia and systemic symptoms (DRESS), Stevens–Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). In recent years, many studies have investigated the immune mechanism and genetic markers of DHRs. Besides, several studies have stated the associations between antibiotics-as well as anti-osteoporotic drugs (AOD)-induced SCARs and specific human leukocyte antigens (HLA) alleles. Strong associations between drugs and HLA alleles such as co-trimoxazole-induced DRESS and HLA-B*13:01 (Odds ratio (OR) = 45), dapsone-DRESS and HLA-B*13:01 (OR = 122.1), vancomycin-DRESS and HLA-A*32:01 (OR = 403), clindamycin-DHRs and HLA-B*15:27 (OR = 55.6), and strontium ranelate (SR)-SJS/TEN and HLA-A*33:03 (OR = 25.97) are listed. We summarized the immune mechanism of SCARs, update the latest knowledge of pharmacogenomics of antibiotics- and AOD-induced SCARs, and indicate the potential clinical use of these genetic markers for SCARs prevention in this mini review article.

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“…Furthermore, ADR also identified to induce hepatic toxicity, called as drug-induced liver injury (DILI). Approximately 10% of DILI patients may progress to acute liver failure ( Yip et al, 2015 ), and the mortality of DILI is up to 7% ( Björnsson and Björnsson, 2017 ). The incidence of DILI is estimated to be 1 to 10 per 100,000 new users ( Yip et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

An Updated Review of Genetic Associations With Severe Adverse Drug Reactions: Translation and Implementation of Pharmacogenomic Testing in Clinical Practice

et al. 2022

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Adverse drug reactions (ADR) remain the major problems in healthcare. Most severe ADR are unpredictable, dose-independent and termed as type B idiosyncratic reactions. Recent pharmacogenomic studies have demonstrated the strong associations between severe ADR and genetic markers, including specific HLA alleles (e.g., HLA-B*15:02/HLA-B*57:01/HLA-A*31:01 for carbamazepine-induced severe cutaneous adverse drug reactions [SCAR], HLA-B*58:01 for allopurinol-SCAR, HLA-B*57:01 for abacavir-hypersensitivity, HLA-B*13:01 for dapsone/co-trimoxazole-induced SCAR, and HLA-A*33:01 for terbinafine-induced liver injury), drug metabolism enzymes (such as CYP2C9*3 for phenytoin-induced SCAR and missense variant of TPMT/NUDT15 for thiopurine-induced leukopenia), drug transporters (e.g., SLCO1B1 polymorphism for statin-induced myopathy), and T cell receptors (Sulfanilamide binding into the CDR3/Vα of the TCR 1.3). This mini review article aims to summarize the current knowledge of pharmacogenomics of severe ADR, and the potentially clinical use of these genetic markers for avoidance of ADR.

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Mortality associated with drug-induced liver injury (DILI)

Cited by 12 publications

References 12 publications

Drug‐Induced Liver Injury in GI Practice

Drug‐Induced Liver Injury in GI Practice

Current understanding of genetic associations with delayed hypersensitivity reactions induced by antibiotics and anti-osteoporotic drugs

An Updated Review of Genetic Associations With Severe Adverse Drug Reactions: Translation and Implementation of Pharmacogenomic Testing in Clinical Practice

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