SynthesisInternational journal of clinical pharmacy2025
Genetic polymorphisms and anti-tuberculosis drug-induced liver injury: an umbrella review of the evidence.
Synthesis in International journal of clinical pharmacy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAnti-tuberculosis drug-induced liver injury (ATLI) is a significant adverse drug reaction with genetic susceptibility implications.
aimThis study aimed to integrate findings from systematic reviews and meta-analyses on genetic polymorphisms associated with ATLI risk, enhance evidence synthesis, and identify susceptibility gene polymorphisms linked to ATLI occurrence.
methodThe protocol was registered in PROSPERO (CRD42024517311). Systematic searches of PubMed, EMBASE, Web of Science, and Cochrane Library databases were conducted to identify eligible studies from inception to February 21, 2024. Two authors independently reviewed eligibility, extracted data, and assessed quality. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate associations between genetic polymorphisms and ATLI susceptibility.
resultsA total of 25 meta-analyses were included, including 57 single nucleotide polymorphisms (SNPs) in 15 candidate genes. Significant associations were found for the glutathione S-transferase M1 (GSTM1) null genotype (OR = 1.43, 95% CI: 1.18-1.73, P < 0.001) and N-acetyltransferase 2 (NAT2) polymorphisms, including rs1799929 (dominant model, OR = 1.35, 95% CI: 1.12-1.63, P < 0.001), rs1799930 (dominant model, OR = 1.43, 95% CI: 1.23-1.66, P < 0.001), rs1799931 (dominant model, OR = 1.22, 95% CI: 1.02-1.46, P = 0.03), and the slow acetylator (SA) phenotype (OR = 2.91, 95% CI: 2.43-3.49, P < 0.001). No significant association was found between the CYP2E1 RsaI/PstI polymorphism (C1/C1 genotype) and ATLI risk (dominant model, OR = 0.79, 95% CI: 0.61-1.02, P = 0.08).
conclusionThis umbrella review confirms that the GSTM1 null genotype, NAT2 polymorphisms (rs1799929, rs1799930, rs1799931), and the slow acetylator phenotype are associated with increased ATLI risk. These findings provide a foundation for further research on genotype-guided approaches to mitigating ATLI.
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