HLA-A*3101 and Carbamazepine-Induced Hypersensitivity Reactions in Europeans

Mark McCormack(Royal College of Surgeons in Ireland), Ana Alfirevic(University of Liverpool), Stéphane Bourgeois(Wellcome Sanger Institute), John Farrell, Dalia Kasperavičiūtė(National Hospital for Neurology and Neurosurgery), Mary Carrington(Ragon Institute of MGH, MIT and Harvard), Graeme J. Sills(University of Liverpool), Tony Marson(University of Liverpool), Xiaoming Jia(Harvard–MIT Division of Health Sciences and Technology), Paul I. W. de Bakker(Broad Institute), Krishna Chinthapalli(National Hospital for Neurology and Neurosurgery), Mariam Molokhia(The King's College), Michael R. Johnson(Imperial College London), Gerard D. O’Connor(Botsford Hospital), Elijah Chaila(Botsford Hospital), Saud Alhusaini(Royal College of Surgeons in Ireland), Kevin V. Shianna, Rodney A. Radtke, Erin L. Heinzen, Nicole Walley, Massimo Pandolfo(Université Libre de Bruxelles), Werner J. Pichler(University of Bern), B. Kevin Park(University of Liverpool), Chantal Depondt(Université Libre de Bruxelles), Sanjay M. Sisodiya(National Hospital for Neurology and Neurosurgery), David B. Goldstein, Panos Deloukas(Wellcome Sanger Institute), Norman Delanty(Royal College of Surgeons in Ireland), Gianpiero L. Cavalleri(Royal College of Surgeons in Ireland), Munir Pirmohamed(University of Liverpool)
New England Journal of Medicine
March 23, 2011
Cited by 912Open Access
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Abstract

BACKGROUND: Carbamazepine causes various forms of hypersensitivity reactions, ranging from maculopapular exanthema to severe blistering reactions. The HLA-B*1502 allele has been shown to be strongly correlated with carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS-TEN) in the Han Chinese and other Asian populations but not in European populations. METHODS: We performed a genomewide association study of samples obtained from 22 subjects with carbamazepine-induced hypersensitivity syndrome, 43 subjects with carbamazepine-induced maculopapular exanthema, and 3987 control subjects, all of European descent. We tested for an association between disease and HLA alleles through proxy single-nucleotide polymorphisms and imputation, confirming associations by high-resolution sequence-based HLA typing. We replicated the associations in samples from 145 subjects with carbamazepine-induced hypersensitivity reactions. RESULTS: The HLA-A*3101 allele, which has a prevalence of 2 to 5% in Northern European populations, was significantly associated with the hypersensitivity syndrome (P=3.5×10(-8)). An independent genomewide association study of samples from subjects with maculopapular exanthema also showed an association with the HLA-A*3101 allele (P=1.1×10(-6)). Follow-up genotyping confirmed the variant as a risk factor for the hypersensitivity syndrome (odds ratio, 12.41; 95% confidence interval [CI], 1.27 to 121.03), maculopapular exanthema (odds ratio, 8.33; 95% CI, 3.59 to 19.36), and SJS-TEN (odds ratio, 25.93; 95% CI, 4.93 to 116.18). CONCLUSIONS: The presence of the HLA-A*3101 allele was associated with carbamazepine-induced hypersensitivity reactions among subjects of Northern European ancestry. The presence of the allele increased the risk from 5.0% to 26.0%, whereas its absence reduced the risk from 5.0% to 3.8%. (Funded by the U.K. Department of Health and others.).


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