HLA-B*59:01: a marker for Stevens–Johnson syndrome/toxic epidermal necrolysis caused by methazolamide in Han Chinese

2015 ◽  
Vol 16 (1) ◽  
pp. 83-87 ◽  
Author(s):  
F Yang ◽  
J Xuan ◽  
J Chen ◽  
H Zhong ◽  
H Luo ◽  
...  
2010 ◽  
Vol 11 (3) ◽  
pp. 349-356 ◽  
Author(s):  
Shuen-Iu Hung ◽  
Wen-Hung Chung ◽  
Zhi-Sheng Liu ◽  
Chien-Hsiun Chen ◽  
Mo-Song Hsih ◽  
...  

2021 ◽  
pp. bjophthalmol-2020-317105
Author(s):  
Kevin Sheng-Kai Ma ◽  
Wen Hung Chung ◽  
Yi-Jen Hsueh ◽  
Shin-Yi Chen ◽  
Katsushi Tokunaga ◽  
...  

Background/aimsStevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) induced by cold medicine (CM) may result in severe ocular complications (SOCs). The purpose of this study was to investigate the human leucocyte antigen (HLA) polymorphism pattern in CM-induced patients with SJS/TEN developing SOCs.MethodsAll participants, including patients with SJS/TEN (n=33) and control patients (n=98), were enrolled through visits to the clinic from 2016 to 2017. SOCs were diagnosed (n=26) via a chart review or eye examination. Patient saliva was collected with commercialised kits and genotyped with PCR assays followed by hybridisation with sequence-specific oligonucleotide (SSO) probes (PCR-SSO) using commercial bead-based typing kits.ResultsIn all patients with SJS/TEN with SOCs, the HLA-A*02:07 carrier frequency was significantly higher than that in controls (OR=3.24, 95% CI=1.09 to 9.60, p=0.049), as was the genotype frequency (OR=3.89, 95% CI=1.49 to 10.16, p=0.007). In patients with CM-SJS/TEN with SOCs, the HLA-A*02:07 carrier frequency was higher than that in controls (OR=5.56, 95% CI=1.52 to 20.00, p=0.016), as was the allele frequency (OR=6.67, 95% CI=2.33 to 20.00, p=0.001). In patients with CM-SJS/TEN with SOCs, the HLA-B*46:01 allele frequency was significantly higher than that in controls (OR=3.85, 95% CI=1.52 to 10.00, p=0.008).ConclusionsThe HLA-A*02:07 and HLA-B*46:01 alleles were significantly associated with SOCs among Han Chinese patients with CM-SJS/TEN. These findings demonstrate the genetic diversity in SJS pathogenesis among different ethnic groups.


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