Polymorphisms in drug metabolism genes as a risk factor for first-line anti-tuberculosis drug-induced liver injury

Background Anti-tuberculosis drug-induced liver injury (AT-DILI) is one of the most common side effects in TB patients during treatment. The prime cause of liver injury during TB treatment is reported to be isoniazid and its metabolites. Different factors influenced the development of AT-DILI, and g...

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Bibliographic Details
Published in:Molecular biology reports 2023-03, Vol.50 (3), p.2893-2900
Main Authors: Meitei, Heikrujam Nilkanta, Pandey, Anupama, Haobam, Reena
Format: Article
Language:English
Subjects:
Alcohol use
Animal Anatomy
Animal Biochemistry
Antitubercular Agents - adverse effects
Arylamine N-Acetyltransferase - genetics
Biomedical and Life Sciences
Chemical and Drug Induced Liver Injury - drug therapy
Chemical and Drug Induced Liver Injury - genetics
Drug metabolism
Drug resistance
Enzymes
Genes
Genetic factors
Histology
HIV
Human immunodeficiency virus
Humans
Isoniazid
Life Sciences
Liver
Metabolism
Metabolites
Mini Review
Molecular biology
Morphology
Polymorphism
Polymorphism, Genetic - genetics
Risk Factors
Tuberculosis
Tuberculosis - drug therapy
Tuberculosis - genetics
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Summary:Background Anti-tuberculosis drug-induced liver injury (AT-DILI) is one of the most common side effects in TB patients during treatment. The prime cause of liver injury during TB treatment is reported to be isoniazid and its metabolites. Different factors influenced the development of AT-DILI, and genetic factors are one of the major factors. Methods and results Polymorphisms in drug metabolism genes like NAT2 , CYP2E1, PXR, and GST have been reported to be associated with AT-DILI, and they are one of the major areas of focus at present. Attempts are met in this review to analyse the different markers in these drug metabolism genes for their association with AT-DILI. Conclusion A better understanding of the polymorphisms in these genes and their functional effects will give better insights into the development of AT-DILI, and it could facilitate in designing and developing more effective personalized treatment for TB.
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-022-08158-7