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
Hauptverfasser: Zhang, Min, Wang, Shuqiang, Wilffert, Bob, Tong, Rongsheng, Soolingen, Dick, Hof, Susan, Alffenaar, Jan‐Willem
Format: Journal Article
Sprache:Englisch
Veröffentlicht: 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.
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
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  surname: Alffenaar
  fullname: Alffenaar, Jan‐Willem
  email: j.w.c.alffenaar@umcg.nl
  organization: University of Groningen, University Medical Center Groningen
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Issue 12
Keywords antituberculosis drug-induced liver injury
meta-analysis
polymorphism
NAT2
Language English
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2011; 26
2007; 3
2008; 64
2011; 25
2014; 9
2014; 94
2003; 167
2003; 41
1976; 84
1995; 50
2015; 16
2010
2015; 94
2017; 27
2013; 40
2002; 35
2008; 56
2017; 174
2012; 39
2005; 49
2011; 6
2007; 13
2006; 86
2011; 106
2016; 3
2005; 366
2017; 12
2016; 20
2016; 63
2016
2016; 61
2011; 45
2016; 60
2015
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2012; 6
2012; 7
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Snippet Aims 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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wiley
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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
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbcp.13722
https://www.ncbi.nlm.nih.gov/pubmed/30047605
https://www.proquest.com/docview/2076911654
https://pubmed.ncbi.nlm.nih.gov/PMC6256008
Volume 84
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