Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Overview

Journal Curr Pharmacol Rep

Date 2018 Nov 23

PMID 30464886

Citations 18

Authors

Yifan Bao

Xiaochao Ma

Theodore P Rasmussen

Xiao-Bo Zhong

Affiliations

Soon will be listed here.

Abstract

Purpose Of This Review: In order to combat the development of drug resistance, the clinical treatment of tuberculosis requires the combined use of several anti-tuberculosis (anti-TB) drugs, including isoniazid and rifampicin. Combinational treatment approaches are suggested by the World Health Organization (WHO) and are widely accepted throughout the world. Unfortunately, a major side effect of the treatment is the development of anti-tuberculosis drug-induced liver injury (AT-DILI). Many factors contribute to isoniazid- and rifampicin-mediated AT-DILI and genetic variations are among the most common factors. The purpose of this review is to provide information on genetic variations associated with isoniazid- and rifampicin-mediated AT-DILI.

Recent Findings: The genetic variations associated with AT-DILI have been identified in the genomic regions within or near genes encoding proteins in the following pathways: drug metabolizing enzymes ( and ), accumulation of bile acids, lipids, and heme metabolites ( and ), immune adaptation ( and ), and oxidant challenge ( and ).

Summary: The information summarized in this review considers the genetic bases of risk factors contributing to AT-DILI and provides information that may help for future studies. Some of the implicated genetic variations can be used in the design of genetic tests and serve as biomarkers for the prediction of isoniazid- and rifampicin-mediated AT-DILI risk in personalized medicine.

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