dc.contributor.author |
Jaramillo-Valverde, Luis |
|
dc.contributor.author |
Levano, Kelly S. |
|
dc.contributor.author |
Tarazona, David D. |
|
dc.contributor.author |
Capristano, Silvia |
|
dc.contributor.author |
Zegarra-Chaponan, Roberto |
|
dc.contributor.author |
Sanchez, Cesar |
|
dc.contributor.author |
Yufra-Picardo, Velia M. |
|
dc.contributor.author |
Tarazona-Santos, Eduardo |
|
dc.contributor.author |
Ugarte Gil, Cesar Augusto |
|
dc.contributor.author |
Guio, Heinner |
|
dc.date.accessioned |
2022-08-15T20:11:08Z |
|
dc.date.available |
2022-08-15T20:11:08Z |
|
dc.date.issued |
2022 |
|
dc.identifier.uri |
https://hdl.handle.net/20.500.12866/12025 |
|
dc.description.abstract |
Background: In Peru, 32,970 people were diagnosed with tuberculosis (TB) in 2019. Although TB treatment is effective, 3.4%–13% is associated with significant adverse drug reactions (ADR), considering drug-induced liver injury (DILI) as the most prevalent. Among the first-line anti-TB drugs, isoniazid (INH) is primarily responsible for the occurrence of DILI. INH is metabolized in the liver by the enzymes N-acetyltransferase-2 (NAT2) and Cytochrome P450 2E1 (CYP2E1). Based on the previous studies, we hypothesized that the interactions between slow CYP2E1 genotype and NAT2 slow acetylators will induce DILI in TB patients. Methods: In this cross-sectional study, all 377 participants completed their anti-TB treatment, and we genotyped SNPs: rs1041983, rs1801280, rs1799929, rs1799930, rs1208, and rs1799931 for NAT2 and rs3813867 and rs2031920 for CYP2E1. Results: We found that rapid, intermediate, and slow NAT2 acetylator were 15%, 38%, and 47%, respectively, in the general population. Intermediate NAT2 acetylator is the least prevalent among patients with adverse reactions (p = 0.024). We did not confirm our hypothesis, however, we found that the combination of intermediate NAT2 acetylators and CYP2E1 c1/c1 genotype significantly protected (OR = 0.16; p = 0.049) against the development of DILI in our population. Conclusion: We propose that the presence of NAT2 intermediate and CYP2E1 c1/c1 genotype could help in therapeutic drug monitoring, and optimize its therapeutic benefits while minimizing its risk for side effects or toxicity. |
en_US |
dc.description.sponsorship |
Este trabajo fue financiado por FONDECYT/CIENCIACTIVA en el marco del programa de Investigación Epidemiológica de la Universidad Peruana Cayetano Heredia [beca EF033-235-2015]. |
es_PE |
dc.language.iso |
eng |
|
dc.publisher |
Wiley |
|
dc.relation.ispartofseries |
Molecular Genetics & Genomic Medicine |
|
dc.rights |
info:eu-repo/semantics/restrictedAccess |
|
dc.rights.uri |
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es |
|
dc.subject |
CYP2E1 |
en_US |
dc.subject |
Hepatotoxicity |
en_US |
dc.subject |
NAT2 |
en_US |
dc.subject |
Tuberculosis |
en_US |
dc.title |
NAT2 and CYP2E1 polymorphisms and antituberculosis drug-induced hepatotoxicity in Peruvian patients |
en_US |
dc.type |
info:eu-repo/semantics/article |
|
dc.identifier.doi |
https://doi.org/10.1002/mgg3.1987 |
|
dc.subject.ocde |
https://purl.org/pe-repo/ocde/ford#1.06.07 |
|
dc.relation.issn |
2324-9269 |
|