Risk of Stevens-Johnson syndrome and toxic epider mal necrolysis during first weeks of antiepileptic therapy: a case-control study

The Lancet ◽  
1999 ◽  
Vol 353 (9171) ◽  
pp. 2190-2194 ◽  
Author(s):  
Berthold Rzany ◽  
Osvaldo Correia ◽  
Judith P Kelly ◽  
Luigi Naldi ◽  
Ariane Auquier ◽  
...  
2021 ◽  
Author(s):  
Francis Capule ◽  
Pramote Tragulpiankit ◽  
Surakameth Mahasirimongkol ◽  
Jiraphun Jittikoon ◽  
Nuanjun Wichukchinda ◽  
...  

Aim: A case-control study was conducted in Filipino patients to determine the association between HLA alleles and carbamazepine-induced Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN). Materials & methods: A retrospective review of medical records and data collection were performed. A total of 10 carbamazepine-induced SJS/TEN cases and 40 tolerant controls were recruited. Genomic DNA extracted from saliva samples was genotyped. Statistical analysis was done. Results: The HLA-B75 serotype (p = 0.003; odds ratio [OR] = 13.8; 95% CI = 2.5–76.8), HLA-B*15:21 (p = 0.041; OR = 4.7; 95% CI = 1.1–20.8) and HLA-A*24:07 (p = 0.032; OR = 6; 95% CI = 1.2–30.7) were significantly associated with carbamazepine-induced SJS/TEN. Conclusion: The HLA-B75 serotype, HLA-B*15:21 or HLA-A*24:07 may be used for pharmacogenetic screening prior to prescribing carbamazepine in Filipinos.


PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68231 ◽  
Author(s):  
Umberto Raucci ◽  
Rossella Rossi ◽  
Roberto Da Cas ◽  
Concita Rafaniello ◽  
Nadia Mores ◽  
...  

2018 ◽  
Vol 45 (9) ◽  
pp. 1080-1087 ◽  
Author(s):  
Fei-Kai Syu ◽  
Hsiu-Yung Pan ◽  
Po-Chun Chuang ◽  
Yi-Syun Huang ◽  
Chi-Yung Cheng ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Chonlaphat Sukasem ◽  
Chonlawat Chaichan ◽  
Thapanat Nakkrut ◽  
Patompong Satapornpong ◽  
Kanoot Jaruthamsophon ◽  
...  

The HLA-B∗15:02 allele has been reported to have a strong association with carbamazepine-induced Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) in Thai patients. The HLA-B alleles associated with carbamazepine-induced maculopapular exanthema (MPE) and the drug reaction with eosinophilia and systemic symptoms (DRESS) among the Thai population have never been reported. The aim of the present study was to carry out an analysis of the involvement of HLA-B alleles in carbamazepine-induced cutaneous adverse drug reactions (cADRs) in the Thai population. A case-control study was performed by genotyping the HLA-B alleles of Thai carbamazepine-induced hypersensitivity reaction patients (17 MPE, 16 SJS/TEN, and 5 DRESS) and 271 carbamazepine-tolerant controls. We also recruited 470 healthy Thai candidate subjects who had not taken carbamazepine. HLA-B∗15:02 showed a significant association with carbamazepine-induced MPE (P=0.0022, odds ratio (OR) (95% confidence interval [CI]) = 7.27 (2.04–25.97)) and carbamazepine-induced SJS/TEN (P=4.46×10−13; OR (95% CI) = 70.91(19.67–255.65)) when compared with carbamazepine-tolerant controls. Carbamazepine-induced SJS/TEN also showed an association with HLA-B∗15:21 allele (P=0.013; OR (95% CI) = 9.54 (1.61–56.57)) when compared with carbamazepine-tolerant controls. HLA-B∗58:01 allele was significantly related to carbamazepine-induced MPE (P=0.007; OR (95% CI) = 4.73 (1.53–14.66)) and DRESS (P=0.0315; OR (95% CI) = 7.55 (1.20–47.58)) when compared with carbamazepine-tolerant controls. These alleles may serve as markers to predict carbamazepine-induced cADRs in the Thai population.


2003 ◽  
Vol 37 (6) ◽  
pp. 812-814 ◽  
Author(s):  
Evagelos N Liberopoulos ◽  
George L Liamis ◽  
Moses S Elisaf

OBJECTIVE: To report a case of possible cefotaxime-induced Stevens–Johnson syndrome (SJS). CASE SUMMARY: A 72-year-old woman with an upper urinary tract infection developed erosions and blisters on the skin and the mucous membranes, as well as fever and prostration, soon after the administration of cefotaxime. This presentation is consistent with the features of SJS. Resolution of the clinical manifestations was observed after discontinuation of the drug; all other drugs, infections, or immunologic disorders that could have caused this syndrome were carefully excluded. An objective causality assessment revealed that SJS was possibly associated with the use of cefotaxime. DISCUSSION: Although cephalosporins have been associated with an increased risk for SJS and cefotaxime has been suspected of being associated with SJS in a previous case–control study, this is the first full report for cefotaxime-related SJS in the literature. An immunologically mediated reaction may be the underlying mechanism. CONCLUSIONS: Although cefotaxime administration seems to be the underlying cause of the SJS observed in our patient, establishment of a definite causal relationship requires additional cases and supportive data.


2016 ◽  
Vol 37 (5) ◽  
pp. 763-767 ◽  
Author(s):  
Selda Keskin Guler ◽  
Bilal Aytac ◽  
Zahide Esra Durak ◽  
Burcu Gokce Cokal ◽  
Nalan Gunes ◽  
...  

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