&lt;I&gt;CYP7A1&lt;/I&gt;, &lt;I&gt;BAAT&lt;/I&gt; and &lt;I&gt;UGT1A1&lt;/I&gt; polymorphisms and susceptibility to anti-tuberculosis drug-induced hepatotoxicity

Chen, R; Wang, Jing; Tang, Shaowen; Zhang, Y; Xz, Lv; Ss, Wu; Zr, Yang; Yy, Xia; Df, Chen; Sy, Zhan

doi:10.5588/ijtld.15.0450

Cited by 13 publications

(20 citation statements)

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“…A SNP (rs3808607) in the CYP7A1 gene is also associated with a higher susceptibility to tuberculosis infection in a Moroccan population [76]. Certain haplotypes in the CYP7A1 gene region have shown a higher risk of AT-DILI in a Chinese patient population [77]. …”

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

“…Although the association of genetic variations in CYP7A1 with AT-DILI has been documented in a Chinese population [77], more population-based studies are needed to establish a solid correlation between the genetic variants of the CYP7A1 gene and AT-DILI.…”

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

“…One study composed of 17 AT-DILI and 71 control patients found a positive association between UGT1A1*27 and UGT1A1*28 (two alleles causing reduced expression of UGT1A1) and an increased risk of AT-DILI [80]. However, other SNPs (rs4148323 and rs8330) in the UGT1A1 gene have no significant correlation with AT-DILI in a study that assessed a Chinese Han population containing 4488 patients [77]. In addition, a recent study examined the relationship between UGT2B7 SNPs and AT-DILI in a Chinese Han population [81].…”

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

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

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

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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 (NAT2, CYP2E1, and GSTs), accumulation of bile acids, lipids, and heme metabolites (CYP7A1, BSEP, UGTs, and PXR), immune adaptation (HLAs and TNF-α), and oxidant challenge (TXNRD1, SOD1, BACH1, and MAFK). 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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Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

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

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

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“…Another recent work conducted in Chinese population has linked CYP7A1 polymorphisms and TB. The authors reported that TB patients carrying an AG genotype of rs1457043 and G–C or G–A haplotypes of rs1457043–rs8192870 in CYP7A1 were at a higher risk to develop anti‐tuberculosis drug‐induced hepatotoxicity (Chen et al., ). Finally, it is recommended that further studies, analysing other genes linked to the CYP7A1 gene, should be designed in conjunction with immunological evaluations that are more complementary.…”

Section: Candidate Genes and The Risk Of Developing Tbmentioning

confidence: 99%

“…were at a higher risk to develop anti-tuberculosis drug-induced hepatotoxicity (Chen et al, 2016). Finally, it is recommended that further studies, analysing other genes linked to the CYP7A1 gene, should be designed in conjunction with immunological evaluations that are more complementary.…”

Section: Cytochrome P450 7a1 (Cyp7a1)mentioning

confidence: 99%

Current immunogenetic predisposition to tuberculosis in the Moroccan population

Qrafli

Najimi

Elaouad

et al. 2017

Int J Immunogenetics

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Tuberculosis (TB) is a serious infectious disease that kills approximately two million people per year, particularly in low- and middle-income countries. Numerous genetic epidemiology studies have been conducted of many ethnic groups worldwide and have highlighted the critical impact of the genetic environment on TB distribution. Many candidate genes associated with resistance or susceptibility to TB have been identified. In Morocco, where TB is still a major public health problem, various observations of clinical, microbiological and incidence distribution are heavily affected by genetic background and external environment. Morocco has almost the same clinical profile as do other North African countries, mainly the increase in more extrapulmonary than pulmonary forms of the diseases, when compared to European, Asian or American populations. In addition, a linkage analysis study that examined Moroccan TB patients identified a unique chromosome region that had a strong association with the risk of contracting TB. Other genes in the Moroccan population that were found to be associated seem to be involved predominantly in modulating the innate immunity. In this review, we appraise the major candidate genes that have been reported in Moroccan immunogenetic studies and discuss their updated role in TB, particularly during the first phase of the immune response to Mycobacterium tuberculosis (Mtb) infection.

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