Volume 8 Supplement 1
Associations of GCLM, gclc and GSTP1 gene polymorphisms and antituberculosis drugs-induced hepatitis
© Kim et al; licensee BioMed Central Ltd. 2015
Published: 8 April 2015
Antituberculosis drugs (ATD) is the most common cause of drug-induce liver injury in many countries. While the mechanism of ATD-induced hepatitis is poorly understood, oxidative stress is suggested to be involved in the development of liver injury to drug metabolites. In this regards, we explored the possible associations between glutathione related enzymes (GCLM, GCLC and GSTP1) gene polymorphisms and ATD-induced hepatitis.
Through regular monitoring of liver function test during the treatment of tuberculosis, 84 patients with ATD-induced hepatitis and 237 ATD-tolerant controls were enrolled. Genotype were assessed in 3 single nucleotide polymorphisms in GCLM (rs41303970, -590T>C), GCLC (rs17883901, -594T>C) and GSTP1 (rs1695, I105V) and compared between case and control groups.
No significant difference was found in genotype frequencies of rs41303970, rs17883901 and rs1695 between patients with ATD-induced hepatitis and ATD-tolerant controls in three statistical models (dominant, recessive and codominant model). In addition, the minor allele frequency were not different between case and control group in three polymorphism sites.
There was no significant association between GCLM, GCLC and GSTP1 gene polymorphisms and ATD-induced hepatitis. These findings suggest that genetic variants of GCLM, GCLC and GSTP1 do not increase the risk of ATD-induced hepatitis.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.