Evidence map›Paper›PMID 24888881›Full record

ArticleEuropean journal of clinical pharmacology2014

N-acetyltransferase 2 (NAT2) genotype as a risk factor for development of drug-induced liver injury relating to antituberculosis drug treatment in a mixed-ethnicity patient group.

Ching-Soon Ng, Abul Hasnat, Abdullah Al Maruf, Maizbha Uddin Ahmed, Munir Pirmohamed, Christopher P Day, Guruprasad P Aithal, Ann K Daly

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Article in European journal of clinical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 4 pooled it
10.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 4 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  3. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease · 2019
    Pooled it
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  19. Mechanism of isoniazid-induced hepatotoxicity: then and now.British journal of clinical pharmacology · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Ching-Soon NgInstitute of Cellular Medicine, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK.
Abul Hasnat
Abdullah Al Maruf
Maizbha Uddin Ahmed
Munir Pirmohamed
Christopher P Day
Guruprasad P Aithal
Ann K Daly
Newcastle University · GBUniversity of Dhaka · BDUniversity of Liverpool · GBUniversity of Nottingham · GB

Funding

Medical Research Council MR/L006758/1
6 · The paper itself

Abstract

purposeThis study aims to assess whether NAT2 genotype affects susceptibility to moderate to severe liver injury in patients undergoing drug treatment for tuberculosis with isoniazid-containing regimens.

methodsTwenty-six patients of European or South Asian ethnicity, who had suffered liver injury during treatment with isoniazid-containing drug regimens and 101 ethnically matched controls were genotyped for the NAT2*5, NAT2*6, and NAT2*7 alleles. Genotyping for additional polymorphisms in the NAT gene region was also performed on 20 of the 26 cases. NAT2 genotype frequency between cases and controls was compared.

resultsNAT2 genotypes predicting a slow acetylator phenotype were found to be associated with an increased risk of isoniazid-related liver injury (odds ratio (OR) = 4.25 (95% confidence interval (CI), 1.36-13.22); p = 0.012) with 85% of the cases being slow acetylators compared with 56% of the controls. There was no evidence for an increased risk for the slow acetylator genotype in patients with the most severe cases of liver injury, who underwent liver transplantation.

conclusionsThe NAT2 slow acetylator genotype appears to be a significant risk factor for moderate and severe drug- induced liver injury. However, the overall effect size is modest and generally in line with effects described previously for this genotype in milder drug-induced liver injury. Additional genetic risk factors may also contribute.

Indexed as

AdultAntitubercular AgentsArylamine N-AcetyltransferaseAsiaCase-Control StudiesChemical and Drug Induced Liver InjuryDrug Therapy, CombinationEthnicityEuropeFemaleGenetic Predisposition to DiseaseGenotypeHumansIsoniazidMaleMiddle AgedAntitubercular AgentsArylamine N-AcetyltransferaseIsoniazidNAT2 protein, human

Identifiers

PMID24888881
OpenAlexW2009165803

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.