scholarly journals NR1I2 genetic polymorphisms and the risk of anti‐tuberculosis drug‐induced hepatotoxicity: A systematic review and meta‐analysis

2020 ◽  
Vol 8 (6) ◽  
Author(s):  
Miaomiao Yang ◽  
Yunliang Qiu ◽  
Yanyu Jin ◽  
Wenpei Liu ◽  
Qingliang Wang ◽  
...  
BMJ Open ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. e027940 ◽  
Author(s):  
Seungwon Yang ◽  
Se Jung Hwang ◽  
Jung Yun Park ◽  
Eun Kyoung Chung ◽  
Jangik I Lee

ObjectivesThe objective of this study was to investigate the association between genetic polymorphisms of N-acetyltransferase 2 (NAT2), cytochrome P450 2E1 (CYP2E1), glutathione S-transferase (GST) and solute carrier organic anion transporter family member 1B1 (SLCO1B1) and the risk of anti-tuberculosis drug-induced liver injury (ATDILI).DesignSystematic review and meta-analysis.Data sourcesPubMed, Embase, Web of Science and Cochrane Reviews databases were searched through April 2019.Eligibility criteriaWe included case-control or cohort studies investigating an association between NAT2, CYP2E1, GST or SLCO1B1 polymorphisms and the ATDILI risk in patients with tuberculosis.Data extraction and synthesisThree authors screened articles, extracted data and assessed study quality. The strength of association was evaluated for each gene using the pooled OR with a 95% CI based on the fixed-effects or random-effects model. Sensitivity analysis was performed to confirm the reliability and robustness of the results.ResultsFifty-four studies were included in this analysis (n=26 for CYP2E1, n=35 for NAT2, n=19 for GST, n=4 for SLCO1B1). The risk of ATDILI was significantly increased with the following genotypes: CYP2E1 RsaI/PstI c1/c1 (OR=1.39, 95% CI 1.06 to 1.83), NAT2 slow acetylator (OR=3.30, 95% CI 2.65 to 4.11) and GSTM1 null (OR=1.30, 95% CI 1.12 to 1.52). No significant association with ATDILI was found for the genetic polymorphisms of CYP2E1 DraI, GSTT1, GSTM1/GSTT1, SLCO1B1 388A>G and SLCO1B1 521T>C (p>0.05).ConclusionsATDILI is more likely to occur in patients with NAT2 slow acetylator genotype, CYP2E1 RsaI/PstI c1/c1 genotype and GSTM1 null genotype. Close monitoring may be warranted for patients with these genotypes.


2021 ◽  
Vol 164 ◽  
pp. 105404
Author(s):  
Hao Niu ◽  
Judith Sanabria-Cabrera ◽  
Ismael Alvarez-Alvarez ◽  
Mercedes Robles-Diaz ◽  
Simona Stankevičiūtė ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Claudia Cristina Biguetti ◽  
Joel Ferreira Santiago Junior ◽  
Matthew William Fiedler ◽  
Mauro Toledo Marrelli ◽  
Marco Brotto

AbstractThe aim of this systematic review was to perform qualitative and quantitative analysis on the toxic effects of chloroquine (CQ) and hydroxychloroquine (HCQ) on skeletal muscles. We designed the study according to PRISMA guidelines. Studies for qualitative and quantitative analyses were selected according to the following inclusion criteria: English language; size of sample (> 5 patients), adult (> age of 18) patients, treated with CQ/HCQ for inflammatory diseases, and presenting and not presenting with toxic effects on skeletal muscles. We collected data published from 1990 to April 2020 using PubMed, Cochrane Library, EMBASE, and SciELO. Risk of bias for observational studies was assessed regarding the ROBIN-I scale. Studies with less than five patients (case reports) were selected for an additional qualitative analysis. We used the software Comprehensive Meta-Analysis at the confidence level of 0.05. We identified 23 studies for qualitative analysis (17 case-reports), and five studies were eligible for quantitative analysis. From case reports, 21 patients presented muscle weakness and confirmatory biopsy for CQ/HCQ induced myopathy. From observational studies, 37 patients out of 1,367 patients from five studies presented muscle weakness related to the use of CQ/HCQ, and 252 patients presented elevated levels of muscle enzymes (aldolase, creatine phosphokinase, and lactate dehydrogenase). Four studies presented data on 34 patients with confirmatory biopsy for drug-induced myopathy. No study presented randomized samples. The chronic use of CQ/HCQ may be a risk for drug-induced myopathy. There is substantiated need for proper randomized trials and controlled prospective studies needed to assess the clinical and subclinical stages of CQ/HCQ -induced muscle myopathy.


2021 ◽  
Vol 26 (1) ◽  
pp. 22
Author(s):  
Nima Rezaei ◽  
MohammadJavad Mousavi ◽  
MohammadReza Hooshangi Shayesteh ◽  
Sirous Jamalzehi ◽  
Reza Alimohammadi ◽  
...  

2017 ◽  
Vol 21 (4) ◽  
pp. 983-994 ◽  
Author(s):  
Esuabom Dijemeni ◽  
Gabriele D’Amone ◽  
Israel Gbati

2016 ◽  
Vol 150 (4) ◽  
pp. S1066
Author(s):  
Sakkarin Chirapongsathorn ◽  
Chayakrit Krittanawong ◽  
Ann M. Farrell ◽  
Mohammad H. Murad ◽  
Patrick Kamath

2014 ◽  
Vol 15 (13) ◽  
pp. 1687-1700 ◽  
Author(s):  
Daniel E Jonas ◽  
Halle R Amick ◽  
Cynthia Feltner ◽  
Roberta Wines ◽  
Ellen Shanahan ◽  
...  

2014 ◽  
Vol 61 (2) ◽  
pp. 220-229 ◽  
Author(s):  
Steven Habbous ◽  
Vincent Pang ◽  
Wei Xu ◽  
Eitan Amir ◽  
Geoffrey Liu

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