ArticleFrontiers in pharmacology2016
HLA-B (*) 58:01 for Allopurinol-Induced Cutaneous Adverse Drug Reactions: Implication for Clinical Interpretation in Thailand.
Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 3 of them syntheses that pooled it.
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Who cites it
45 citing papers in PubMed, 3 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- HLA-B*58:01 genotyping prevalence and the association with allopurinol-induced severe cutaneous adverse reactions: a living systematic review and meta-analysis.Scientific reports · 2025Pooled it
- Diagnostic Test Criteria for HLA Genotyping to Prevent Drug Hypersensitivity Reactions: A Systematic Review of Actionable HLA Recommendations in CPIC and DPWG Guidelines.Frontiers in pharmacology · 2020Pooled it
- Impact of HLA-B*58:01 allele and allopurinol-induced cutaneous adverse drug reactions: evidence from 21 pharmacogenetic studies.Oncotarget · 2016Pooled it
- A Post-NGP Mitsuokella jalaludinii as a Therapeutic Candidate for Gout.MicrobiologyOpen · 2026Article
- Development of a non-genetic risk prediction model for allopurinol-induced severe cutaneous adverse drug reactions: a multicenter retrospective observational study.Clinical rheumatology · 2026Observational
- Assessing willingness to pay for HLA-B*58:01 genetic testing before allopurinol initiation and its potential impact on future health policy, Thailand.Scientific reports · 2026Article
- Prospective longitudinal study of psychological sequelae, self-perception of body image, and quality of life in severe cutaneous adverse drug reactions: a case-control study.Frontiers in medicine · 2026Article
- Research progress on potential high-risk drugs for Stevens-Johnson syndrome and toxic epidermal necrolysis with insights from adverse drug reaction database mining.Frontiers in pharmacology · 2026Review
- HLA‒B*58:01 and skin reactions in pediatric hematology and oncology patients treated with allopurinol.Clinical and experimental pediatrics · 2025Article
- An Updated Economic Evaluation of HLA-B*58:01 Genotype Testing in Gouty Patients for Preventing Severe Allopurinol Hypersensitivity in Thailand.ACR open rheumatology · 2025Article
- Updates in the pathogenesis of SJS/TEN.Allergology international : official journal of the Japanese Society of Allergology · 2025Review
- A Phase I Dose-Escalation Study of the Pharmacokinetics, Pharmacodynamics, and Safety of a Single Oral Dose of Tigulixostat.Drug design, development and therapy · 2025Article
- Pharmacogenomic landscape of the Thai population from genome sequencing of 949 individuals.Scientific reports · 2024Article
- Severe cutaneous adverse reactions.Nature reviews. Disease primers · 2024Review
- Influence of pharmacogenomic polymorphisms on allopurinol-induced cutaneous adverse drug reactions in Thai patients.BMC medical genomics · 2024Article
- HLA-B*57:01-dependent intracellular stress in keratinocytes triggers dermal hypersensitivity reactions to abacavir.PNAS nexus · 2024Article
- Article
- Delayed Drug Hypersensitivity Reactions: Molecular Recognition, Genetic Susceptibility, and Immune Mediators.Biomedicines · 2023Review
- Ultrarapid and high-resolution HLA class I typing using transposase-based nanopore sequencing applied in pharmacogenetic testing.Frontiers in genetics · 2023Article
- Genotypic and Phenotypic Characteristics of Co-Trimoxazole-Induced Cutaneous Adverse Reactions.Dermatology (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study was to investigate the predisposition to different types of allopurinol-induced cutaneous adverse drug reactions (CADR), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN; SJS-TEN, n = 13), drug reaction with eosinophilia and systemic symptoms (DRESS, n = 10) and Maculopapular eruption (MPE; n = 7), conferred by HLA-B (*) 58:01 in a Thai population.
methodsThis case-control association study compares 30 patients with allopurinol-induced CADR, allopurinol-tolerant control patients (n = 100), and a Thai general population (n = 1095). Patients' human leukocyte antigen type B (HLA-B) alleles were genotyped by using a two-stage sequence-specific oligonucleotide probe system.
resultsOf a total 30 patients with CADR due to allopurinol, 29 (96.7%) patients were found to be at least heterozygous for HLA-B (*) 58:01, compared to only 4.0% in allopurinol-tolerant patients (p < 0.001). Odds ratio (OR) for the association of HLA-B (*) 58:01 with allopurinol-induced CADR in this population was 696.0 (95% CI: 74.8-6475.0). The HLA-B (*) 58:01 allele was present in all patients with allopurinol-induced SJS-TEN (OR = 579.0, 95%CI: 29.5-11362.7, p < 0.001) and DRESS (OR 430.3, 95%CI: 22.6-8958.9, p < 0.001). Additionally, OR of HLA-B (*) 58:01 was highly significant in the allopurinol-induced MPE patients (OR 144.0, 95%CI: 13.9-1497.0, p < 0.001).
conclusionIn this study we confirmed the association between HLAB (*) 58:01 and allopurinol-induced SJS-TEN in a Thai population. In addition, we identified an association between HLA-B (*) 58:01 and allopurinol-induced DRESS and MPE in this population. Therefore, HLA-B (*) 58:01 can be used as a pharmacogenetic marker for allopurinol-induced CADR including SJS-TEN, DRESS and MPE. These results suggest that screening for HLA-B (*) 58:01 alleles in patients who will be treated with allopurinol would be clinically helpful in preventing the risk of developing CARD in a Thai patients. Summary Regardless of phenotype, this is the first pharmacogenetic study of allopurinol-induced CADR in patients of Thai ancestry.In this study we confirmed the association between HLA-B (*) 58:01 and allopurinol-induced SJS-TEN, DRESS, and MPE in Thai population.Regarding to our findings, the pharmacogenetic interpretation could be generalized to drug hypersensitivity including DRESS, SJS-TEN, and MPE.
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