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<p>It has been proposed that mitochondrial DNA variations can affect mitochondrial function, increasing the risk of drug-induced liver injury. This study aims to explore the association between mitochondrial DNA (mtDNA) variants and anti-tuberculosis drug-induced liver injury (ATT_DILI) in Korean tuberculosis patients. Whole mitochondrial genomes from 185 patients (61 with ATT_DILI and 124 without liver injury) were sequenced. Comparative analyses examined mtDNA variants, variant counts, and haplogroups between the two groups, adjusted with Bonferroni correction. The m.16189 T &gt; C variant, associated with reduced mtDNA copy number, was more frequent in ATT_DILI cases (39.3%) than in controls (29.0%). Logistic regression suggested a potential association (odds ratio 4.92, 95% confidence interval 1.14–21.23, <i>p</i> = 0.033), though this significance was lost after correction. No significant differences in mtDNA variant counts or haplogroups were observed between groups. While mtDNA variants and haplogroups appear to have a limited role in predicting ATT_DILI risk, the m.16189 T &gt; C variant warrants further investigation.</p>

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Mitochondrial DNA variants and susceptibility to anti-tuberculosis drug-induced liver injury in Korean patients

  • 期刊论文

  • 发表日期：

    2025年10月29日

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  • Vinh Hoa Pham,
  • Sang-Heon Kim,
  • Young-Koo Jee,
  • Tae-Won Jang,
  • Jinsoo Min,
  • Ho-Sook Kim,
  • Yong-Soon Cho,
  • Jae-Gook Shin

摘要

It has been proposed that mitochondrial DNA variations can affect mitochondrial function, increasing the risk of drug-induced liver injury. This study aims to explore the association between mitochondrial DNA (mtDNA) variants and anti-tuberculosis drug-induced liver injury (ATT_DILI) in Korean tuberculosis patients. Whole mitochondrial genomes from 185 patients (61 with ATT_DILI and 124 without liver injury) were sequenced. Comparative analyses examined mtDNA variants, variant counts, and haplogroups between the two groups, adjusted with Bonferroni correction. The m.16189 T > C variant, associated with reduced mtDNA copy number, was more frequent in ATT_DILI cases (39.3%) than in controls (29.0%). Logistic regression suggested a potential association (odds ratio 4.92, 95% confidence interval 1.14–21.23, p = 0.033), though this significance was lost after correction. No significant differences in mtDNA variant counts or haplogroups were observed between groups. While mtDNA variants and haplogroups appear to have a limited role in predicting ATT_DILI risk, the m.16189 T > C variant warrants further investigation.