Whole genome sequencing identifies genetic variants associated with co-trimoxazole hypersensitivity in Asians
Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic...
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| Published in | Journal of allergy and clinical immunology Vol. 147; no. 4; pp. 1402 - 1412 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.04.2021
Elsevier Limited |
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| Online Access | Get full text |
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| Abstract | Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole–induced SCAR remains unclear.
We aimed to investigate the genetic predisposition of co-trimoxazole–induced SCAR.
We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole–induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.
The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole–induced SCAR (P = 8.2 × 10−9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole–related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole–induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10−21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10−5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole–induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10−23; OR = 40.1).
This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole–induced SCAR in Asians. |
|---|---|
| AbstractList | Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole–induced SCAR remains unclear.
We aimed to investigate the genetic predisposition of co-trimoxazole–induced SCAR.
We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole–induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.
The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole–induced SCAR (P = 8.2 × 10−9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole–related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole–induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10−21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10−5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole–induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10−23; OR = 40.1).
This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole–induced SCAR in Asians. Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear. We aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR. We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia. The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10 ; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10 ; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10 ; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10 ; OR = 40.1). This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians. Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear.BACKGROUNDCo-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear.We aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR.OBJECTIVEWe aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR.We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.METHODSWe conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10-9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10-21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10-5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10-23; OR = 40.1).RESULTSThe whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10-9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10-21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10-5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10-23; OR = 40.1).This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians.CONCLUSIONThis study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians. BackgroundCo-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole–induced SCAR remains unclear.ObjectiveWe aimed to investigate the genetic predisposition of co-trimoxazole–induced SCAR.MethodsWe conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole–induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia.ResultsThe whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole–induced SCAR (P = 8.2 × 10−9; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole–related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole–induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10−21; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10−5; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole–induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10−23; OR = 40.1).ConclusionThis study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole–induced SCAR in Asians. |
| Author | Teng, Yu-Chuan Konyoung, Parinya Lee, Yun-Shien Tassaneeyakul, Wichittra Chung, Wen-Hung Choon, Siew-Eng Rerknimitr, Pawinee Hui, Rosaline Chung-Yee Lin, Shang-Hung Hung, Shuen-Iu Lin, Yang Yu-Wei Chang, Chee-Jen Klaewsongkram, Jettanong Chiu, Tsu-Man Lu, Chun-Wei Rerkpattanapipat, Ticha Huang, Cheng-Yang Chang, Ya-Ching Chantratita, Wasun Chan, Cheng-Chi Lee, Chaw-Ning Sukasem, Chonlaphat Chen, Wei-Ti Wang, Chuang-Wei Amornpinyo, Warayuwadee Huang, Yu Huei Chen, Chun-Bing Saksit, Niwat Huang, Yen-Hua Lin, Yu-Jr Nakkam, Nontaya Hsu, Chao-Kai |
| Author_xml | – sequence: 1 givenname: Chuang-Wei surname: Wang fullname: Wang, Chuang-Wei organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 2 givenname: Wichittra surname: Tassaneeyakul fullname: Tassaneeyakul, Wichittra organization: Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand – sequence: 3 givenname: Chun-Bing surname: Chen fullname: Chen, Chun-Bing organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 4 givenname: Wei-Ti surname: Chen fullname: Chen, Wei-Ti organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 5 givenname: Yu-Chuan surname: Teng fullname: Teng, Yu-Chuan organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 6 givenname: Cheng-Yang surname: Huang fullname: Huang, Cheng-Yang organization: School of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan – sequence: 7 givenname: Chonlaphat surname: Sukasem fullname: Sukasem, Chonlaphat organization: Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand – sequence: 8 givenname: Chun-Wei surname: Lu fullname: Lu, Chun-Wei organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 9 givenname: Yun-Shien surname: Lee fullname: Lee, Yun-Shien organization: Department of Biotechnology, Ming Chuan University, Taoyuan, Taiwan – sequence: 10 givenname: Siew-Eng surname: Choon fullname: Choon, Siew-Eng organization: Hospital Sultanah Aminah, Clinical School Johor Bahru, Jeffrey Cheah School of Medicine and Health Sciences, Monash University, Selangor, Malaysia – sequence: 11 givenname: Nontaya surname: Nakkam fullname: Nakkam, Nontaya organization: Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand – sequence: 12 givenname: Rosaline Chung-Yee surname: Hui fullname: Hui, Rosaline Chung-Yee organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 13 givenname: Yen-Hua surname: Huang fullname: Huang, Yen-Hua organization: School of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan – sequence: 14 givenname: Ya-Ching surname: Chang fullname: Chang, Ya-Ching organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 15 givenname: Yang Yu-Wei surname: Lin fullname: Lin, Yang Yu-Wei organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 16 givenname: Chee-Jen surname: Chang fullname: Chang, Chee-Jen organization: Research Services Center for Health Information, Chang Gung University, Taoyuan, Taiwan – sequence: 17 givenname: Tsu-Man surname: Chiu fullname: Chiu, Tsu-Man organization: Department of Dermatology, Changhua Christian Hospital, Changhua, Taiwan – sequence: 18 givenname: Wasun surname: Chantratita fullname: Chantratita, Wasun organization: Center of Medical Genomics, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand – sequence: 19 givenname: Parinya surname: Konyoung fullname: Konyoung, Parinya organization: Pharmacy Unit, Udon Thani Hospital, Udon Thani, Thailand – sequence: 20 givenname: Chaw-Ning surname: Lee fullname: Lee, Chaw-Ning organization: Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan – sequence: 21 givenname: Jettanong surname: Klaewsongkram fullname: Klaewsongkram, Jettanong organization: Thai Severe Cutaneous Adverse Drug Reaction Research Group, Thailand – sequence: 22 givenname: Ticha surname: Rerkpattanapipat fullname: Rerkpattanapipat, Ticha organization: Thai Severe Cutaneous Adverse Drug Reaction Research Group, Thailand – sequence: 23 givenname: Warayuwadee surname: Amornpinyo fullname: Amornpinyo, Warayuwadee organization: Division of Dermatology, Department of Internal Medicine, Khon Kaen Hospital, Khon Kaen, Thailand – sequence: 24 givenname: Niwat surname: Saksit fullname: Saksit, Niwat organization: Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand – sequence: 25 givenname: Pawinee surname: Rerknimitr fullname: Rerknimitr, Pawinee organization: Thai Severe Cutaneous Adverse Drug Reaction Research Group, Thailand – sequence: 26 givenname: Yu Huei surname: Huang fullname: Huang, Yu Huei organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 27 givenname: Shang-Hung surname: Lin fullname: Lin, Shang-Hung organization: Department of Dermatology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan – sequence: 28 givenname: Chao-Kai surname: Hsu fullname: Hsu, Chao-Kai organization: Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan – sequence: 29 givenname: Cheng-Chi surname: Chan fullname: Chan, Cheng-Chi organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan – sequence: 30 givenname: Yu-Jr surname: Lin fullname: Lin, Yu-Jr organization: Research Services Center for Health Information, Chang Gung University, Taoyuan, Taiwan – sequence: 31 givenname: Shuen-Iu surname: Hung fullname: Hung, Shuen-Iu email: sihung@cgmh.org.tw, hungshueniu@gmail.com organization: Cancer Vaccine and Immune Cell Therapy Core Laboratory, Chang Gung Memorial Hospital, Linkou, Taiwan – sequence: 32 givenname: Wen-Hung orcidid: 0000-0003-1681-0959 surname: Chung fullname: Chung, Wen-Hung email: wenhungchung@yahoo.com, chung1@cgmh.org.tw organization: Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taipei, and Keelung, Taiwan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32791162$$D View this record in MEDLINE/PubMed |
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| Copyright | 2020 American Academy of Allergy, Asthma & Immunology Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. 2020. American Academy of Allergy, Asthma & Immunology |
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| Keywords | WGS OR Co-trimoxazole whole-genome sequencing GSTP1 SCAR HLA-B∗13:01 EEF2 MPO GCLC DRESS SNP sulfonamide NAT2 NPV PPV IRB TEN SJS severe hypersensitivity reactions LAT MICA |
| Language | English |
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| Snippet | Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis... BackgroundCo-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for... |
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| SubjectTerms | Acetyltransferase Acquired immune deficiency syndrome AIDS Antibiotics Causality Co-trimoxazole Cotrimoxazole CYP2D6 protein Cytochrome P450 Eosinophilia Ethics Genetic diversity Genomes Genotyping Glutathione transferase Histocompatibility antigen HLA HIV HLA-B∗13:01 Hospitals Human immunodeficiency virus Hypersensitivity Infections Infectious diseases Lymphocytes Mortality N-Acetyltransferase 2 Patients Phenotypes Pneumonia Population Principal components analysis Prophylaxis severe hypersensitivity reactions Single-nucleotide polymorphism Statistical analysis Stevens-Johnson syndrome sulfonamide Sulfonamides Toxic epidermal necrolysis Urogenital system Whole genome sequencing |
| Title | Whole genome sequencing identifies genetic variants associated with co-trimoxazole hypersensitivity in Asians |
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