Huyen Tran Thi, Phuc Nguyen Hoang, Phuong Pham Thi Minh, Vinh Nguyen Thi Ha, Son Dao Anh
{"title":"HLA-A*02:07与磺胺甲恶唑-甲氧苄啶致药疹的关系","authors":"Huyen Tran Thi, Phuc Nguyen Hoang, Phuong Pham Thi Minh, Vinh Nguyen Thi Ha, Son Dao Anh","doi":"10.5455/msm.2025.37.111-116","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Fixed drug eruption (FDE) is an adverse drug reaction that recurs at the same site upon re-exposure to the triggering medication. Sulfonamide antibiotics, especially sulfamethoxazole-trimethoprim, are common causes of FDE. Previous studies have linked drug hypersensitivity reactions to specific human leukocyte antigens (HLA).</p><p><strong>Objective: </strong>This study aimed to investigate the association between HLA-A and FDE induced by sulfamethoxazole-trimethoprim.</p><p><strong>Methods: </strong>A cross-sectional study was conducted with 30 FDE patients and 30 healthy controls who had tolerated sulfamethoxazole-trimethoprim. Blood samples (3 ml) were collected for HLA-A typing using polymerase chain reaction with sequence-specific oligonucleotides (PCR-SSO).</p><p><strong>Results: </strong>Twenty-three HLA-A alleles were detected. In the FDE group, the alleles with high frequency were HLA-A*02:07 (12 patients; 40%), HLA-A*11:01 (10 patients; 33.3%), and HLA-A*24:02 (6 patients; 20%). In the control group, the most commonly observed alleles were HLA-A*11:01 (12 patients; 40%), HLA-A*24:02 (6 patients; 20%), HLA-A*24:07 (6 patients; 20%), HLA-A*29:01 (6 patients; 20%), and HLA-A*33:03 (9 patients; 30%). The FDE group had a higher frequency of HLA-A*02:07 than the control group (40% vs. 16.67%, p < 0.05). No differences in the frequencies of other HLA-A alleles were observed between the two groups. Participants with the HLA-A*02:07 allele were 3.33 times more likely to develop FDE caused by sulfamethoxazole-trimethoprim compared to those without the allele (OR = 3.33, 95% CI: 1.09 - 11.14).</p><p><strong>Conclusion: </strong>The study suggests an association between the HLA-A*02:07 allele and FDE induced by sulfamethoxazole-trimethoprim in the Vietnamese population. Screening for HLA-A*02:07 prior to prescribing sulfamethoxazole-trimethoprim could help identify at-risk individuals and prevent FDE.</p>","PeriodicalId":94128,"journal":{"name":"Materia socio-medica","volume":"37 2","pages":"111-116"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12212223/pdf/","citationCount":"0","resultStr":"{\"title\":\"Association Between HLA-A*02:07 and Fixed Drug Eruption Caused by Sulfamethoxazole-Trimethoprim.\",\"authors\":\"Huyen Tran Thi, Phuc Nguyen Hoang, Phuong Pham Thi Minh, Vinh Nguyen Thi Ha, Son Dao Anh\",\"doi\":\"10.5455/msm.2025.37.111-116\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Fixed drug eruption (FDE) is an adverse drug reaction that recurs at the same site upon re-exposure to the triggering medication. Sulfonamide antibiotics, especially sulfamethoxazole-trimethoprim, are common causes of FDE. Previous studies have linked drug hypersensitivity reactions to specific human leukocyte antigens (HLA).</p><p><strong>Objective: </strong>This study aimed to investigate the association between HLA-A and FDE induced by sulfamethoxazole-trimethoprim.</p><p><strong>Methods: </strong>A cross-sectional study was conducted with 30 FDE patients and 30 healthy controls who had tolerated sulfamethoxazole-trimethoprim. Blood samples (3 ml) were collected for HLA-A typing using polymerase chain reaction with sequence-specific oligonucleotides (PCR-SSO).</p><p><strong>Results: </strong>Twenty-three HLA-A alleles were detected. In the FDE group, the alleles with high frequency were HLA-A*02:07 (12 patients; 40%), HLA-A*11:01 (10 patients; 33.3%), and HLA-A*24:02 (6 patients; 20%). In the control group, the most commonly observed alleles were HLA-A*11:01 (12 patients; 40%), HLA-A*24:02 (6 patients; 20%), HLA-A*24:07 (6 patients; 20%), HLA-A*29:01 (6 patients; 20%), and HLA-A*33:03 (9 patients; 30%). The FDE group had a higher frequency of HLA-A*02:07 than the control group (40% vs. 16.67%, p < 0.05). No differences in the frequencies of other HLA-A alleles were observed between the two groups. Participants with the HLA-A*02:07 allele were 3.33 times more likely to develop FDE caused by sulfamethoxazole-trimethoprim compared to those without the allele (OR = 3.33, 95% CI: 1.09 - 11.14).</p><p><strong>Conclusion: </strong>The study suggests an association between the HLA-A*02:07 allele and FDE induced by sulfamethoxazole-trimethoprim in the Vietnamese population. 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引用次数: 0
摘要
背景:固定药疹(FDE)是一种药物不良反应,在同一部位再次暴露于触发药物后复发。磺胺类抗生素,特别是磺胺甲恶唑-甲氧苄啶,是FDE的常见原因。先前的研究将药物过敏反应与特定的人类白细胞抗原(HLA)联系起来。目的:探讨磺胺甲恶唑-甲氧苄啶诱导的HLA-A与FDE的关系。方法:对30例FDE患者和30例耐受磺胺甲恶唑-甲氧苄啶的健康对照者进行横断面研究。采集血样(3ml),采用序列特异性寡核苷酸聚合酶链反应(PCR-SSO)进行HLA-A分型。结果:检出HLA-A等位基因23个。FDE组高频等位基因为HLA-A*02:07(12例);40%), HLA-A*11:01(10例;33.3%), HLA-A*24:02(6例;20%)。对照组中最常见的等位基因为HLA-A*11:01(12例;40%), HLA-A*24:02(6例;20%), HLA-A*24:07(6例;20%), HLA-A*29:01(6例;20%), HLA-A*33:03(9例;30%)。FDE组HLA-A*02:07阳性率高于对照组(40% vs. 16.67%, p < 0.05)。其他HLA-A等位基因的频率在两组之间没有差异。携带HLA-A*02:07等位基因的参与者发生磺胺甲恶唑-甲氧苄啶引起的FDE的可能性是不携带该等位基因的参与者的3.33倍(OR = 3.33, 95% CI: 1.09 - 11.14)。结论:越南人群HLA-A*02:07等位基因与磺胺甲恶唑-甲氧苄啶致FDE存在相关性。在处方磺胺甲恶唑-甲氧苄啶之前筛查HLA-A*02:07有助于识别高危人群并预防FDE。
Association Between HLA-A*02:07 and Fixed Drug Eruption Caused by Sulfamethoxazole-Trimethoprim.
Background: Fixed drug eruption (FDE) is an adverse drug reaction that recurs at the same site upon re-exposure to the triggering medication. Sulfonamide antibiotics, especially sulfamethoxazole-trimethoprim, are common causes of FDE. Previous studies have linked drug hypersensitivity reactions to specific human leukocyte antigens (HLA).
Objective: This study aimed to investigate the association between HLA-A and FDE induced by sulfamethoxazole-trimethoprim.
Methods: A cross-sectional study was conducted with 30 FDE patients and 30 healthy controls who had tolerated sulfamethoxazole-trimethoprim. Blood samples (3 ml) were collected for HLA-A typing using polymerase chain reaction with sequence-specific oligonucleotides (PCR-SSO).
Results: Twenty-three HLA-A alleles were detected. In the FDE group, the alleles with high frequency were HLA-A*02:07 (12 patients; 40%), HLA-A*11:01 (10 patients; 33.3%), and HLA-A*24:02 (6 patients; 20%). In the control group, the most commonly observed alleles were HLA-A*11:01 (12 patients; 40%), HLA-A*24:02 (6 patients; 20%), HLA-A*24:07 (6 patients; 20%), HLA-A*29:01 (6 patients; 20%), and HLA-A*33:03 (9 patients; 30%). The FDE group had a higher frequency of HLA-A*02:07 than the control group (40% vs. 16.67%, p < 0.05). No differences in the frequencies of other HLA-A alleles were observed between the two groups. Participants with the HLA-A*02:07 allele were 3.33 times more likely to develop FDE caused by sulfamethoxazole-trimethoprim compared to those without the allele (OR = 3.33, 95% CI: 1.09 - 11.14).
Conclusion: The study suggests an association between the HLA-A*02:07 allele and FDE induced by sulfamethoxazole-trimethoprim in the Vietnamese population. Screening for HLA-A*02:07 prior to prescribing sulfamethoxazole-trimethoprim could help identify at-risk individuals and prevent FDE.