Abstract:This study suggests that the acetylator status of TB patients can be detected by phenotypic method as efficaciously as by genotypic method. Therefore, phenotypic method can replace genotypic method to determine acetylating status as phenotypic method is simple and inexpensive.
“…, Rana et al . and Rana et al . were excluded due to overlap with their other studies (we therefore selected the later publication to analyse the distribution of the NAT2 genotype); three studies, by Guaoua et al .…”
Section: Resultsmentioning
confidence: 90%
“…The main characteristics of the 37 studies are shown in Table 1. The studies by An et al [15], Rana et al [16] and Rana et al [17] were excluded due to overlap with their other studies (we therefore selected the later publication to analyse the distribution of the NAT2 genotype); three studies, by Guaoua et al [18], Ng [19] and Mishra et al [20], were excluded as controls were not TB patients but healthy people; the studies by Roy et al [21] and Cavaco et al [22] were excluded due to the absence of complete NAT2 polymorphism distribution data. The study by Ohno et al [23] was excluded due to the absence of slow acetylators.…”
Section: Identification and Characteristics Of The Included Studiesmentioning
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).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).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, I
2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41–17.10, I
2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58–9.24, I
2 = 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.
“…, Rana et al . and Rana et al . were excluded due to overlap with their other studies (we therefore selected the later publication to analyse the distribution of the NAT2 genotype); three studies, by Guaoua et al .…”
Section: Resultsmentioning
confidence: 90%
“…The main characteristics of the 37 studies are shown in Table 1. The studies by An et al [15], Rana et al [16] and Rana et al [17] were excluded due to overlap with their other studies (we therefore selected the later publication to analyse the distribution of the NAT2 genotype); three studies, by Guaoua et al [18], Ng [19] and Mishra et al [20], were excluded as controls were not TB patients but healthy people; the studies by Roy et al [21] and Cavaco et al [22] were excluded due to the absence of complete NAT2 polymorphism distribution data. The study by Ohno et al [23] was excluded due to the absence of slow acetylators.…”
Section: Identification and Characteristics Of The Included Studiesmentioning
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).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).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, I
2 = 51.3%, P = 0.000). The OR varied between different ethnic populations, ranging from 6.42 (95% CI 2.41–17.10, I
2 = 2.3%) for the West Asian population to 2.32 (95% CI 0.58–9.24, I
2 = 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.
“…We contacted several study authors for clarification. For two articles,51,68 we did not receive a response and, consequently, data from the older article68 were excluded from a meta-analysis to which both articles contributed data. If the two articles reported data for two distinct cohorts, then information would have been lost by excluding one article.…”
(TB) patients receiving anti-tuberculosis treatment may experience serious adverse drug reactions (ADRs) such as hepatotoxicity. Variants of the N-acetyltransferase 2 (NAT2) gene may increase the risk of experiencing such toxicity events. O B J E C T I V E : To provide a comprehensive evaluation of the evidence base for associations between NAT2 variants and anti-tuberculosis drug-related toxicity. M E T H O D : This was a systematic review and metaanalysis. We searched for studies in Medline, PubMed, EMBASE, BIOSIS and Web of Science. We included data from 41 articles (39 distinct cohorts of patients). We pooled effect estimates for each genotype on each outcome using meta-analyses stratified by country.
“…Their study showed that the differences in the NAT2 slow‐acetylator allele frequencies were not statistically significant between cases and controls. In our previous study, we observed that the acetylator status of patients with TB can be detected by phenotypic method as efficaciously as by genotypic method. In the present study, we observed that NAT2 4/4, 4/5 and 4/7 alleles (fast acetylators) were not significantly different in ATT‐induced hepatotoxicity patients as compared to the non‐hepatotoxicity group, whereas NAT2 5/7 and 6/7 (slow acetylators) were significantly higher in hepatotoxicity patients as compared to the non‐hepatotoxicity group.…”
This study indicates that patients with slow-acetylator genotypes (NAT2 5/7, 6/7) and GSTM1 allele of GST enzyme were at higher risk of ATT-induced hepatotoxicity.
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