Literature DB >> 24888881

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 Ng1, Abul Hasnat, Abdullah Al Maruf, Maizbha Uddin Ahmed, Munir Pirmohamed, Christopher P Day, Guruprasad P Aithal, Ann K Daly.   

Abstract

PURPOSE: This 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.
METHODS: Twenty-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.
RESULTS: NAT2 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.
CONCLUSIONS: The 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.

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Year:  2014        PMID: 24888881     DOI: 10.1007/s00228-014-1703-0

Source DB:  PubMed          Journal:  Eur J Clin Pharmacol        ISSN: 0031-6970            Impact factor:   2.953


  47 in total

1.  Serum transaminase elevations and other hepatic abnormalities in patients receiving isoniazid.

Authors:  L Scharer; J P Smith
Journal:  Ann Intern Med       Date:  1969-12       Impact factor: 25.391

2.  Inhibition of isoniazid-induced hepatotoxicity in rabbits by pretreatment with an amidase inhibitor.

Authors:  T C Sarich; S P Adams; G Petricca; J M Wright
Journal:  J Pharmacol Exp Ther       Date:  1999-05       Impact factor: 4.030

3.  NAT2 and CYP2E1 polymorphisms and susceptibility to first-line anti-tuberculosis drug-induced hepatitis.

Authors:  S-W Lee; L S-C Chung; H-H Huang; T-Y Chuang; Y-H Liou; L S-H Wu
Journal:  Int J Tuberc Lung Dis       Date:  2010-05       Impact factor: 2.373

4.  Polymorphism of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatotoxicity in Tunisian patients with tuberculosis.

Authors:  L Ben Mahmoud; H Ghozzi; A Kamoun; A Hakim; H Hachicha; S Hammami; Z Sahnoun; N Zalila; H Makni; K Zeghal
Journal:  Pathol Biol (Paris)       Date:  2012-10

5.  Comparison between acetylator phenotype and genotype polymorphism of n-acetyltransferase-2 in tuberculosis patients.

Authors:  S V Rana; R P Ola; Sanjeev K Sharma; S K Arora; S K Sinha; P Pandhi; K Singh
Journal:  Hepatol Int       Date:  2011-08-25       Impact factor: 6.047

6.  Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses?

Authors:  Martina Kinzig-Schippers; Dorota Tomalik-Scharte; Alexander Jetter; Bernhard Scheidel; Verena Jakob; Michael Rodamer; Ingolf Cascorbi; Oxana Doroshyenko; Fritz Sörgel; Uwe Fuhr
Journal:  Antimicrob Agents Chemother       Date:  2005-05       Impact factor: 5.191

7.  Determining the relation between N-acetyltransferase-2 acetylator phenotype and antituberculosis drug induced hepatitis by molecular biologic tests.

Authors:  Vildan Bozok Cetintaş; Onur Fevzi Erer; Buket Kosova; Ilker Ozdemir; Nejat Topçuoğlu; Serir Aktoğu; Zuhal Eroğlu
Journal:  Tuberk Toraks       Date:  2008

8.  Hepatic adducts, circulating antibodies, and cytokine polymorphisms in patients with diclofenac hepatotoxicity.

Authors:  Guruprasad P Aithal; Lesley Ramsay; Ann K Daly; Nhareet Sonchit; Julian B S Leathart; Graeme Alexander; J Gerald Kenna; John Caldwell; Christopher P Day
Journal:  Hepatology       Date:  2004-05       Impact factor: 17.425

9.  Sex, ethnicity, and slow acetylator profile are the major causes of hepatotoxicity induced by antituberculosis drugs.

Authors:  Julián G Chamorro; Jorge P Castagnino; Rosa M Musella; Mabel Nogueras; Federico M Aranda; Ana Frías; Mabel Visca; Omar Aidar; Silvia Perés; Gabriela F de Larrañaga
Journal:  J Gastroenterol Hepatol       Date:  2013-02       Impact factor: 4.029

10.  N-acetyltransferase (NAT2) polymorphism and breast cancer susceptibility: a lack of association in a case-control study of Turkish population.

Authors:  Neslihan Aygün Kocabaş; Semra Sardaş; Suzanne Cholerton; Ann K Daly; Ali Esat Karakaya
Journal:  Int J Toxicol       Date:  2004 Jan-Feb       Impact factor: 2.032

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  14 in total

Review 1.  Oxidative Stress and First-Line Antituberculosis Drug-Induced Hepatotoxicity.

Authors:  Wing Wai Yew; Kwok Chiu Chang; Denise P Chan
Journal:  Antimicrob Agents Chemother       Date:  2018-07-27       Impact factor: 5.191

2.  NAT2 variants and toxicity related to anti-tuberculosis agents: a systematic review and meta-analysis.

Authors:  M Richardson; J Kirkham; K Dwan; D J Sloan; G Davies; A L Jorgensen
Journal:  Int J Tuberc Lung Dis       Date:  2019-03-01       Impact factor: 2.373

3.  Genetic Polymorphisms of SLCO1B1, CYP2E1 and UGT1A1 and Susceptibility to Anti-Tuberculosis Drug-Induced Hepatotoxicity: A Chinese Population-Based Prospective Case-Control Study.

Authors:  Qin Sun; Hai-Peng Liu; Rui-Juan Zheng; Peng Wang; Zhi-Bin Liu; Wei Sha; He-Ping Xiao
Journal:  Clin Drug Investig       Date:  2017-12       Impact factor: 2.859

Review 4.  Mechanism of isoniazid-induced hepatotoxicity: then and now.

Authors:  Imir Metushi; Jack Uetrecht; Elizabeth Phillips
Journal:  Br J Clin Pharmacol       Date:  2016-02-25       Impact factor: 4.335

5.  Deficiency of N-acetyltransferase increases the interactions of isoniazid with endobiotics in mouse liver.

Authors:  Pengcheng Wang; Amina I Shehu; Jie Lu; Rujuta H Joshi; Raman Venkataramanan; Kim S Sugamori; Denis M Grant; Xiao-Bo Zhong; Xiaochao Ma
Journal:  Biochem Pharmacol       Date:  2017-09-06       Impact factor: 5.858

6.  NAT2 gene polymorphism: covert drug interaction causing phenytoin toxicity.

Authors:  C Adithan; A Subathra
Journal:  Indian J Med Res       Date:  2016-05       Impact factor: 2.375

7.  A Physiologically Based Pharmacokinetic Model of Isoniazid and Its Application in Individualizing Tuberculosis Chemotherapy.

Authors:  Henrik Cordes; Christoph Thiel; Hélène E Aschmann; Vanessa Baier; Lars M Blank; Lars Kuepfer
Journal:  Antimicrob Agents Chemother       Date:  2016-09-23       Impact factor: 5.191

Review 8.  Are Polymorphisms in Genes Relevant to Drug Disposition Predictors of Susceptibility to Drug-Induced Liver Injury?

Authors:  Ann K Daly
Journal:  Pharm Res       Date:  2016-12-27       Impact factor: 4.200

9.  Integration of genome-scale metabolic networks into whole-body PBPK models shows phenotype-specific cases of drug-induced metabolic perturbation.

Authors:  Henrik Cordes; Christoph Thiel; Vanessa Baier; Lars M Blank; Lars Kuepfer
Journal:  NPJ Syst Biol Appl       Date:  2018-02-26

Review 10.  Impact of New Genomic Technologies on Understanding Adverse Drug Reactions.

Authors:  Simran D S Maggo; Ruth L Savage; Martin A Kennedy
Journal:  Clin Pharmacokinet       Date:  2016-04       Impact factor: 6.447

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