Genetic Variants Associated with Non-Steroidal Anti-Inflammatory Drug-Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

<b>Background/Objectives</b>: Non-steroidal anti-inflammatory drugs (NSAIDs) are widely prescribed to help alleviate pain and treat inflammation, but they are also recognized as common causes of severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Despite their clinical importance, pharmacogenetic markers to predict individual susceptibility to NSAID-induced SJS/TEN remain insufficiently defined. This study investigated associations between <i>HLA</i> class I and II alleles, <i>CYP2C9</i> polymorphisms, and NSAID-induced SJS/TEN in a Thai population. <b>Methods</b>: A total of 18 patients with NSAID-induced SJS/TEN and 54 NSAID-tolerant controls were enrolled. Genotype data from 183 unrelated Thai individuals without a history of drug allergy were included as a general population control group. Genotyping was performed for <i>HLA</i> class I and II alleles and the <i>CYP2C9*3</i> variant. <b>Results</b>: <i>HLA-DQB1*03:02</i> was significantly associated with NSAID-induced SJS/TEN (OR = 9.23, 95% CI = 2.19-38.83, <i>p</i> = 0.0024, Pc = 0.0312), particularly those triggered by piroxicam (OR = 13.71, 95% CI = 2.81-66.86, <i>p</i> = 0.0012, Pc = 0.0156). Additional associations were identified for <i>HLA-B*56:01</i> and <i>HLA-A*68:01</i> in the overall NSAID-induced SJS/TEN group. The subgroup analysis suggested that these alleles, along with <i>HLA-DRB1*04:03</i>, were associated with an increased risk of piroxicam-induced SJS/TEN. However, these associations did not remain statistically significant after Bonferroni's correction. No significant association was identified for <i>CYP2C9*3</i>. <b>Conclusions</b>: This study identified specific <i>HLA</i> alleles, particularly <i>HLA-DQB1*03:02</i>, as candidate pharmacogenetic risk factors for NSAID-induced SJS/TEN in a Thai population, especially in piroxicam-associated cases. However, these associations should be considered exploratory. Larger, multicenter, multi-ethnic studies are required to validate these findings and clarify their potential clinical utility.

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Journal
Medical Sciences
Published
2026-02-19
DOI
https://doi.org/10.3390/medsci14010098
Primary Topic
Drug-Induced Adverse Reactions
Type
article
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article

Genetic Variants Associated with Non-Steroidal Anti-Inflammatory Drug-Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

Danklai Purimart, S Kanjanawart, Nontaya Nakkam, Warayuwadee Amornpinyo et al.
Medical Sciences
Drug-Induced Adverse Reactions
article

Genetic Variants Associated with Non-Steroidal Anti-Inflammatory Drug-Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

Danklai Purimart, S Kanjanawart, Nontaya Nakkam, Warayuwadee Amornpinyo, Parinya Konyoung, Tassaneeyakul Wichittra, Jenita Kosanlawit, Oranuch Pattanacheewapull
article en

Abstract

<b>Background/Objectives</b>: Non-steroidal anti-inflammatory drugs (NSAIDs) are widely prescribed to help alleviate pain and treat inflammation, but they are also recognized as common causes of severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Despite their clinical importance, pharmacogenetic markers to predict individual susceptibility to NSAID-induced SJS/TEN remain insufficiently defined. This study investigated associations between <i>HLA</i> class I and II alleles, <i>CYP2C9</i> polymorphisms, and NSAID-induced SJS/TEN in a Thai population. <b>Methods</b>: A total of 18 patients with NSAID-induced SJS/TEN and 54 NSAID-tolerant controls were enrolled. Genotype data from 183 unrelated Thai individuals without a history of drug allergy were included as a general population control group. Genotyping was performed for <i>HLA</i> class I and II alleles and the <i>CYP2C9*3</i> variant. <b>Results</b>: <i>HLA-DQB1*03:02</i> was significantly associated with NSAID-induced SJS/TEN (OR = 9.23, 95% CI = 2.19-38.83, <i>p</i> = 0.0024, Pc = 0.0312), particularly those triggered by piroxicam (OR = 13.71, 95% CI = 2.81-66.86, <i>p</i> = 0.0012, Pc = 0.0156). Additional associations were identified for <i>HLA-B*56:01</i> and <i>HLA-A*68:01</i> in the overall NSAID-induced SJS/TEN group. The subgroup analysis suggested that these alleles, along with <i>HLA-DRB1*04:03</i>, were associated with an increased risk of piroxicam-induced SJS/TEN. However, these associations did not remain statistically significant after Bonferroni's correction. No significant association was identified for <i>CYP2C9*3</i>. <b>Conclusions</b>: This study identified specific <i>HLA</i> alleles, particularly <i>HLA-DQB1*03:02</i>, as candidate pharmacogenetic risk factors for NSAID-induced SJS/TEN in a Thai population, especially in piroxicam-associated cases. However, these associations should be considered exploratory. Larger, multicenter, multi-ethnic studies are required to validate these findings and clarify their potential clinical utility.

Medical SciencesVol. 14(1)
Khon Kaen University (TH), Udon Thani Hospital (TH)
Khon Kaen University
Good health and well-being
Openalex Percentile: Top 50%
Drug-Induced Adverse Reactions
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