The association between the NAT2 genetic polymorphisms and risk of DILI during anti‐TB treatment: a systematic review and meta‐analysis
Aims The aim of this study is to evaluate the potential association between N‐acetyltransferase type 2 (NAT2) polymorphisms and drug‐induced liver injury during anti‐TB treatment (AT‐DILI). Methods We conducted a systematic review and performed a meta‐analysis to clarify the role of NAT2 polymorphis...
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| Veröffentlicht in: | British journal of clinical pharmacology Jg. 84; H. 12; S. 2747 - 2760 |
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| Hauptverfasser: | , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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England
John Wiley and Sons Inc
01.12.2018
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| ISSN: | 0306-5251, 1365-2125, 1365-2125 |
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| Abstract | Aims
The aim of this study is to evaluate the potential association between N‐acetyltransferase type 2 (NAT2) polymorphisms and drug‐induced liver injury during anti‐TB treatment (AT‐DILI).
Methods
We conducted a systematic review and performed a meta‐analysis to clarify the role of NAT2 polymorphism in AT‐DILI. PubMed, Medline and EMBASE databases were searched for studies published in English to December 31, 2017, on the association between the NAT2 polymorphism and AT‐DILI risk. Outcomes were pooled with random‐effects meta‐analysis. Details were registered in the PROSPERO register (number: CRD42016051722).
Results
Thirty‐seven studies involving 1527 cases and 7184 controls were included in this meta‐analysis. The overall odds ratio (OR) of AT‐DILI associated with NAT2 slow acetylator phenotype was 3.15 (95% CI 2.58–3.84, I2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41–17.10, I2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58–9.24, I2 = 80.3%) for the European population. Within the slow NAT2 genotype, variation was also observed; NAT2*6/*7 was associated with the highest risk of AT‐DILI (OR = 1.68, 95% CI 1.09–2.59) compared to the other slow NAT2 acetylators combined.
Conclusions
NAT2 slow acetylation was observed to increase the risk of AT‐DILI in tuberculosis patients. Our results support the hypothesis that the slow NAT2 genotype is a risk factor for AT‐DILI. |
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| AbstractList | The aim of this study is to evaluate the potential association between N-acetyltransferase type 2 (NAT2) polymorphisms and drug-induced liver injury during anti-TB treatment (AT-DILI).
We conducted a systematic review and performed a meta-analysis to clarify the role of NAT2 polymorphism in AT-DILI. PubMed, Medline and EMBASE databases were searched for studies published in English to December 31, 2017, on the association between the NAT2 polymorphism and AT-DILI risk. Outcomes were pooled with random-effects meta-analysis. Details were registered in the PROSPERO register (number: CRD42016051722).
Thirty-seven studies involving 1527 cases and 7184 controls were included in this meta-analysis. The overall odds ratio (OR) of AT-DILI associated with NAT2 slow acetylator phenotype was 3.15 (95% CI 2.58-3.84, I
= 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41-17.10, I
= 2.3%) for the West Asian population to 2.32 (95% CI 0.58-9.24, I
= 80.3%) for the European population. Within the slow NAT2 genotype, variation was also observed; NAT2*6/*7 was associated with the highest risk of AT-DILI (OR = 1.68, 95% CI 1.09-2.59) compared to the other slow NAT2 acetylators combined.
NAT2 slow acetylation was observed to increase the risk of AT-DILI in tuberculosis patients. Our results support the hypothesis that the slow NAT2 genotype is a risk factor for AT-DILI. The aim of this study is to evaluate the potential association between N-acetyltransferase type 2 (NAT2) polymorphisms and drug-induced liver injury during anti-TB treatment (AT-DILI).AIMSThe aim of this study is to evaluate the potential association between N-acetyltransferase type 2 (NAT2) polymorphisms and drug-induced liver injury during anti-TB treatment (AT-DILI).We conducted a systematic review and performed a meta-analysis to clarify the role of NAT2 polymorphism in AT-DILI. PubMed, Medline and EMBASE databases were searched for studies published in English to December 31, 2017, on the association between the NAT2 polymorphism and AT-DILI risk. Outcomes were pooled with random-effects meta-analysis. Details were registered in the PROSPERO register (number: CRD42016051722).METHODSWe conducted a systematic review and performed a meta-analysis to clarify the role of NAT2 polymorphism in AT-DILI. PubMed, Medline and EMBASE databases were searched for studies published in English to December 31, 2017, on the association between the NAT2 polymorphism and AT-DILI risk. Outcomes were pooled with random-effects meta-analysis. Details were registered in the PROSPERO register (number: CRD42016051722).Thirty-seven studies involving 1527 cases and 7184 controls were included in this meta-analysis. The overall odds ratio (OR) of AT-DILI associated with NAT2 slow acetylator phenotype was 3.15 (95% CI 2.58-3.84, I2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41-17.10, I2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58-9.24, I2 = 80.3%) for the European population. Within the slow NAT2 genotype, variation was also observed; NAT2*6/*7 was associated with the highest risk of AT-DILI (OR = 1.68, 95% CI 1.09-2.59) compared to the other slow NAT2 acetylators combined.RESULTSThirty-seven studies involving 1527 cases and 7184 controls were included in this meta-analysis. The overall odds ratio (OR) of AT-DILI associated with NAT2 slow acetylator phenotype was 3.15 (95% CI 2.58-3.84, I2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41-17.10, I2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58-9.24, I2 = 80.3%) for the European population. Within the slow NAT2 genotype, variation was also observed; NAT2*6/*7 was associated with the highest risk of AT-DILI (OR = 1.68, 95% CI 1.09-2.59) compared to the other slow NAT2 acetylators combined.NAT2 slow acetylation was observed to increase the risk of AT-DILI in tuberculosis patients. Our results support the hypothesis that the slow NAT2 genotype is a risk factor for AT-DILI.CONCLUSIONSNAT2 slow acetylation was observed to increase the risk of AT-DILI in tuberculosis patients. Our results support the hypothesis that the slow NAT2 genotype is a risk factor for AT-DILI. Aims The aim of this study is to evaluate the potential association between N‐acetyltransferase type 2 (NAT2) polymorphisms and drug‐induced liver injury during anti‐TB treatment (AT‐DILI). Methods We conducted a systematic review and performed a meta‐analysis to clarify the role of NAT2 polymorphism in AT‐DILI. PubMed, Medline and EMBASE databases were searched for studies published in English to December 31, 2017, on the association between the NAT2 polymorphism and AT‐DILI risk. Outcomes were pooled with random‐effects meta‐analysis. Details were registered in the PROSPERO register (number: CRD42016051722). Results Thirty‐seven studies involving 1527 cases and 7184 controls were included in this meta‐analysis. The overall odds ratio (OR) of AT‐DILI associated with NAT2 slow acetylator phenotype was 3.15 (95% CI 2.58–3.84, I2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41–17.10, I2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58–9.24, I2 = 80.3%) for the European population. Within the slow NAT2 genotype, variation was also observed; NAT2*6/*7 was associated with the highest risk of AT‐DILI (OR = 1.68, 95% CI 1.09–2.59) compared to the other slow NAT2 acetylators combined. Conclusions NAT2 slow acetylation was observed to increase the risk of AT‐DILI in tuberculosis patients. Our results support the hypothesis that the slow NAT2 genotype is a risk factor for AT‐DILI. |
| Author | Soolingen, Dick Wilffert, Bob Hof, Susan Tong, Rongsheng Wang, Shuqiang Alffenaar, Jan‐Willem Zhang, Min |
| AuthorAffiliation | 5 Personalized Drug Therapy Key Laboratory of Sichuan Province 3 Department of Infectious Diseases Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital Chengdu China 4 Department of Pharmacotherapy, ‐Epidemiology, & ‐Economics, Groningen Research Institute of Pharmacy University of Groningen Groningen The Netherlands 8 KNCV Tuberculosis Foundation The Hague The Netherlands 1 Department of Pharmacy Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital Chengdu China 7 Department of Medical Microbiology Radboud University Medical Centre Nijmegen The Netherlands 6 Tuberculosis Reference Laboratory National Institute for Public Health and the Environment (RIVM) Bilthoven The Netherlands 2 University of Groningen, University Medical Center Groningen Department of Clinical Pharmacy and Pharmacology Groningen The Netherlands |
| AuthorAffiliation_xml | – name: 3 Department of Infectious Diseases Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital Chengdu China – name: 8 KNCV Tuberculosis Foundation The Hague The Netherlands – name: 1 Department of Pharmacy Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital Chengdu China – name: 2 University of Groningen, University Medical Center Groningen Department of Clinical Pharmacy and Pharmacology Groningen The Netherlands – name: 5 Personalized Drug Therapy Key Laboratory of Sichuan Province – name: 7 Department of Medical Microbiology Radboud University Medical Centre Nijmegen The Netherlands – name: 6 Tuberculosis Reference Laboratory National Institute for Public Health and the Environment (RIVM) Bilthoven The Netherlands – name: 4 Department of Pharmacotherapy, ‐Epidemiology, & ‐Economics, Groningen Research Institute of Pharmacy University of Groningen Groningen The Netherlands |
| Author_xml | – sequence: 1 givenname: Min surname: Zhang fullname: Zhang, Min organization: University of Groningen, University Medical Center Groningen – sequence: 2 givenname: Shuqiang surname: Wang fullname: Wang, Shuqiang organization: Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital – sequence: 3 givenname: Bob orcidid: 0000-0002-8759-5697 surname: Wilffert fullname: Wilffert, Bob organization: University of Groningen – sequence: 4 givenname: Rongsheng surname: Tong fullname: Tong, Rongsheng organization: Personalized Drug Therapy Key Laboratory of Sichuan Province – sequence: 5 givenname: Dick surname: Soolingen fullname: Soolingen, Dick organization: Radboud University Medical Centre – sequence: 6 givenname: Susan surname: Hof fullname: Hof, Susan organization: KNCV Tuberculosis Foundation – sequence: 7 givenname: Jan‐Willem orcidid: 0000-0001-6703-0288 surname: Alffenaar fullname: Alffenaar, Jan‐Willem email: j.w.c.alffenaar@umcg.nl organization: University of Groningen, University Medical Center Groningen |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30047605$$D View this record in MEDLINE/PubMed |
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| Copyright | 2018 The Authors. British Journal of Clinical Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society. |
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| Keywords | antituberculosis drug-induced liver injury meta-analysis polymorphism NAT2 |
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The aim of this study is to evaluate the potential association between N‐acetyltransferase type 2 (NAT2) polymorphisms and drug‐induced liver injury... The aim of this study is to evaluate the potential association between N-acetyltransferase type 2 (NAT2) polymorphisms and drug-induced liver injury during... |
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| SubjectTerms | Antitubercular Agents - adverse effects antituberculosis drug‐induced liver injury Arylamine N-Acetyltransferase - genetics Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - genetics Genetic Predisposition to Disease Genotype Humans meta‐analysis NAT2 polymorphism Polymorphism, Genetic Review |
| Title | The association between the NAT2 genetic polymorphisms and risk of DILI during anti‐TB treatment: a systematic review and meta‐analysis |
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