Association of Liver Injury From Specific Drugs, or Groups of Drugs, With Polymorphisms in HLA and Other Genes in a Genome-Wide Association Study
We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases...
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| Published in | Gastroenterology (New York, N.Y. 1943) Vol. 152; no. 5; pp. 1078 - 1089 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.04.2017
Elsevier |
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| Online Access | Get full text |
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| Abstract | We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors.
We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs.
We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9−3.8; P = 2.4 × 10−8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6−2.5; P = 9.7 × 10−9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6−2.7; P = 4.8 × 10−9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0−9.5; P = 7.1 × 10−9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224.
In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non−drug-specific risk factors. |
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| AbstractList | We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors.
We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs.
We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9−3.8; P = 2.4 × 10−8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6−2.5; P = 9.7 × 10−9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6−2.7; P = 4.8 × 10−9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0−9.5; P = 7.1 × 10−9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224.
In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non−drug-specific risk factors. We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors.BACKGROUND & AIMSWe performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors.We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs.METHODSWe performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs.We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9-3.8; P = 2.4 × 10-8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6-2.5; P = 9.7 × 10-9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6-2.7; P = 4.8 × 10-9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0-9.5; P = 7.1 × 10-9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224.RESULTSWe associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9-3.8; P = 2.4 × 10-8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6-2.5; P = 9.7 × 10-9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6-2.7; P = 4.8 × 10-9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0-9.5; P = 7.1 × 10-9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224.In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors.CONCLUSIONSIn a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors. Background & Aims We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. Methods We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. Results We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9−3.8; P = 2.4 × 10−8 ) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6−2.5; P = 9.7 × 10−9 ). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6−2.7; P = 4.8 × 10−9 ). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0−9.5; P = 7.1 × 10−9 ). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. Conclusions In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non−drug-specific risk factors. BACKGROUND & AIMS:We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors.METHODS:We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs.RESULTS:We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9-3.8; P = 2.4 × 10-8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6-2.5; P = 9.7 × 10-9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6-2.7; P = 4.8 × 10-9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0-9.5; P = 7.1 × 10-9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224.CONCLUSIONS:In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors. BACKGROUND & AIMS: We performed a genome-wide association study (GWAS) to identify genetic risk factors for druginduced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. METHODS: We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. RESULTS: We associated DILI with rs114577328 (a proxy for A* 33: 01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9 - 3.8; P = 2.4 x 10(-8)) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6 - 2.5; P = 9.7 x 10(-9)). The association with A* 33: 01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A* 33: 01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6 - 2.7; P = 4.8 x 10(-9)). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0 - 9.5; P = 7.1 x 10(-9)). We validated the association between A* 33: 01 terbinafine-and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. CONCLUSIONS: In a GWAS of persons of European descent with DILI, we associated HLA-A* 33: 01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors. We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9-3.8; P = 2.4 × 10 ) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6-2.5; P = 9.7 × 10 ). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6-2.7; P = 4.8 × 10 ). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0-9.5; P = 7.1 × 10 ). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors. |
| Author | Sawle, Ashley Serrano, Jose Stolz, Andrew Nelson, Matthew R. Molokhia, Mariam Fontana, Robert J. Chalasani, Naga Conforti, Anita Barnhart, Huiman X. Bessone, Fernando Carvajal, Alfonso Hernández, Nelia Coulthard, Sally A. Martin, Jennifer H. Hallberg, Pär Bjornsson, Einar S. Andrade, Raul J. Shen, Yufeng Stephens, Camilla Kullak-Ublick, Gerd A. Cascorbi, Ingolf Bondon-Guitton, Emmanuelle Pirmohamed, Munir Floratos, Aris Urban, Thomas J. Hayashi, Paul H. Daly, Mark J. Lucena, M. Isabel Maitland-van der Zee, Anke H. Nicoletti, Paola Cirulli, Elizabeth T. Day, Christopher P. Grove, Jane I. Aithal, Guruprasad P. Powell, Elizabeth E. Daly, Ann K. Larrey, Dominique Ibáñez, Luisa Watkins, Paul B. Dillon, John F. Wadelius, Mia Laitinen, Tarja Qin, Shengying Arrese, Marco |
| AuthorAffiliation | 16 Medical Research Institute, University of Dundee,Ninewells Hospital, Dundee, UK 34 UNC Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina 10 Universidad de Valladolid, Valladolid, Spain 22 Clinical Research Unit for Pulmonary Diseases, Helsinki University Central Hospital, Helsinki, Finland 33 Target Sciences, GSK, King of Prussia, Pennsylvania 7 Universite de Toulouse, Toulouse, France 19 Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay 31 University of Southern California, Los Angeles, California 18 Department of Medical Sciences and Science for Life Laboratory, Uppsala University, Uppsala, Sweden 25 School of Medicine and Public Health, University of Newcastle, New South Wales, Australia 21 Department of Clinical Pharmacology and Toxicology, University Hospital and University of Zurich, Zurich, Switzerland 11 Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Kiel, Germany 12 Division of Gastr |
| AuthorAffiliation_xml | – name: 19 Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay – name: 21 Department of Clinical Pharmacology and Toxicology, University Hospital and University of Zurich, Zurich, Switzerland – name: 7 Universite de Toulouse, Toulouse, France – name: 32 University of North Carolina Institute for Drug Safety Sciences, Eshelman School of Pharmacy, North Carolina – name: 22 Clinical Research Unit for Pulmonary Diseases, Helsinki University Central Hospital, Helsinki, Finland – name: 24 Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht University, Utrecht, Netherlands – name: 27 Department of Molecular and Clinical Pharmacology, University of Liverpool, Liverpool, UK – name: 12 Division of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, Indiana – name: 6 Duke University, Durham, North Carolina – name: 1 Department of Systems Biology, Columbia University, New York – name: 11 Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Kiel, Germany – name: 33 Target Sciences, GSK, King of Prussia, Pennsylvania – name: 34 UNC Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina – name: 30 National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland – name: 2 National Institute for Health Research (NIHR) Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospital NHS Trust and University of Nottingham, Nottingham, UK – name: 4 UGC Digestivo, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Universitario Virgen de la Victoria, Universidad de Málaga, Málaga, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) – name: 29 Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Shanghai Jiao Tong University, Shanghai, China – name: 5 Departmento de Gastroenterología, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile – name: 20 Fundació Institut Català de Farmacologia, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain – name: 28 Centre for Liver Disease Research, School of Medicine, The University of Queensland, Brisbane, QLD, Australia – name: 25 School of Medicine and Public Health, University of Newcastle, New South Wales, Australia – name: 31 University of Southern California, Los Angeles, California – name: 3 Department of Internal Medicine, Landspitali University Hospital, Reykjavik, Iceland – name: 8 Department of Internal Medicine, University of North Carolina – Chapel Hill, North Carolina – name: 18 Department of Medical Sciences and Science for Life Laboratory, Uppsala University, Uppsala, Sweden – name: 10 Universidad de Valladolid, Valladolid, Spain – name: 23 Liver Unit, CHU St Eloi Hospital, Montpellier, France – name: 14 Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK – name: 15 Broad Institute of Harvard and MIT, Boston – name: 26 Department of Primary Care and Public Health Sciences, King's College, London, UK – name: 16 Medical Research Institute, University of Dundee,Ninewells Hospital, Dundee, UK – name: 9 Servicio de Gastroenterología y Hepatología, Universidad Nacional de Rosario, Rosario, Argentina – name: 13 University Hospital, Verona, Italy – name: 17 University of Michigan, Ann Arbor, Michigan |
| Author_xml | – sequence: 1 givenname: Paola surname: Nicoletti fullname: Nicoletti, Paola organization: Department of Systems Biology, Columbia University, New York, New York – sequence: 2 givenname: Guruprasad P. surname: Aithal fullname: Aithal, Guruprasad P. organization: National Institute for Health Research, Nottingham Digestive Diseases Biomedical Research Unit, Nottingham University Hospital, National Health Service Trust, and University of Nottingham, Nottingham, United Kingdom – sequence: 3 givenname: Einar S. surname: Bjornsson fullname: Bjornsson, Einar S. organization: Department of Internal Medicine, Landspitali University Hospital, Reykjavik, Iceland – sequence: 4 givenname: Raul J. surname: Andrade fullname: Andrade, Raul J. organization: Unidad de Gestión Clínica Digestivo, Instituto de Investigación Biomédica de Málaga, Hospital Universitario Virgen de la Victoria, Universidad de Málaga, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Málaga, Spain – sequence: 5 givenname: Ashley surname: Sawle fullname: Sawle, Ashley organization: Department of Systems Biology, Columbia University, New York, New York – sequence: 6 givenname: Marco surname: Arrese fullname: Arrese, Marco organization: Departmento de Gastroenterología, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile – sequence: 7 givenname: Huiman X. surname: Barnhart fullname: Barnhart, Huiman X. organization: Duke University, Durham, North Carolina – sequence: 8 givenname: Emmanuelle surname: Bondon-Guitton fullname: Bondon-Guitton, Emmanuelle organization: Universite de Toulouse, Toulouse, France – sequence: 9 givenname: Paul H. surname: Hayashi fullname: Hayashi, Paul H. organization: Department of Internal Medicine, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina – sequence: 10 givenname: Fernando surname: Bessone fullname: Bessone, Fernando organization: Servicio de Gastroenterología y Hepatología, Universidad Nacional de Rosario, Rosario, Argentina – sequence: 11 givenname: Alfonso surname: Carvajal fullname: Carvajal, Alfonso organization: Universidad de Valladolid, Valladolid, Spain – sequence: 12 givenname: Ingolf surname: Cascorbi fullname: Cascorbi, Ingolf organization: Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Kiel, Germany – sequence: 13 givenname: Elizabeth T. surname: Cirulli fullname: Cirulli, Elizabeth T. organization: Duke University, Durham, North Carolina – sequence: 14 givenname: Naga surname: Chalasani fullname: Chalasani, Naga organization: Division of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, Indiana – sequence: 15 givenname: Anita surname: Conforti fullname: Conforti, Anita organization: University Hospital, Verona, Italy – sequence: 16 givenname: Sally A. surname: Coulthard fullname: Coulthard, Sally A. organization: Institute of Cellular Medicine, 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University of Nottingham, Nottingham, United Kingdom – sequence: 22 givenname: Pär surname: Hallberg fullname: Hallberg, Pär organization: Department of Medical Sciences and Science for Life Laboratory, Uppsala University, Uppsala, Sweden – sequence: 23 givenname: Nelia surname: Hernández fullname: Hernández, Nelia organization: Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay – sequence: 24 givenname: Luisa surname: Ibáñez fullname: Ibáñez, Luisa organization: Fundació Institut Català de Farmacologia, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain – sequence: 25 givenname: Gerd A. surname: Kullak-Ublick fullname: Kullak-Ublick, Gerd A. organization: Department of Clinical Pharmacology and Toxicology, University Hospital and University of Zurich, Zurich, Switzerland – sequence: 26 givenname: Tarja surname: Laitinen fullname: Laitinen, Tarja organization: Clinical Research Unit for Pulmonary Diseases, Helsinki University 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| Snippet | We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without... Background & Aims We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs... BACKGROUND & AIMS:We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs... BACKGROUND & AIMS: We performed a genome-wide association study (GWAS) to identify genetic risk factors for druginduced liver injury (DILI) from licensed... |
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| SubjectTerms | Alleles Anti-Fungal Agent Antidepressive Agents - adverse effects Antifungal Agents - adverse effects Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - genetics Chromosomes, Human, Pair 2 - genetics Female Fenofibrate - adverse effects Gastroenterology and Hepatology Genes, MHC Class I - genetics Genetic Predisposition to Disease Genome-Wide Association Study HLA-A Antigens - genetics Human health and pathology Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects Hypolipidemic Agents - adverse effects Hépatology and Gastroenterology Life Sciences Liver Damage Male Medication Middle Aged Naphthalenes - adverse effects Odds Ratio Phenotype Platelet Aggregation Inhibitors - adverse effects Polymorphism, Single Nucleotide Sertraline - adverse effects Side Effect Terbinafine Ticlopidine - adverse effects White People - genetics |
| Title | Association of Liver Injury From Specific Drugs, or Groups of Drugs, With Polymorphisms in HLA and Other Genes in a Genome-Wide Association Study |
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