Antituberculosis drugs and hepatotoxicity among hospitalized patients in Jos, Nigeria

Isa, Samson Ejiji; Ebonyi, Augustine O.; Shehu, Nathan Y.; Idoko, Patrick; Anejo-Okopi, Joseph; Gomerep, Simji Samuel; Odesanya, Rachael U.; Abah, Isaac Okoh; Jimoh, Hafsat O

doi:10.1016/j.ijmyco.2015.10.001

Cited by 26 publications

(26 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In this present research, hepatotoxicity was observed in 6.9% of control group participants on only the antitubercular medicines, lower than 18.2% reported by Isa et al. (). Hepatotoxicity is caused by isoniazid and rifampicin in patients (Devarbhavi et al.…”

Section: Discussioncontrasting

confidence: 77%

Methionine and vitamin B‐complex ameliorate antitubercular drugs‐induced toxicity in exposed patients

Amagon

Awodele

Akindele

2017

Pharmacology Res & Perspec

View full text Add to dashboard Cite

Tuberculosis therapy utilizes drugs that while effective cause treatment‐related toxicity. Modulation of antitubercular drugs‐induced toxicity by methionine and vitamin B‐complex in patients was evaluated. 285 treatment‐naïve tuberculosis patients at the Chest Clinics of Infectious Diseases Hospital, Yaba and General Hospital, Lagos in Lagos, Nigeria was prospectively recruited and allotted into test (antitubercular medicines, methionine and vitamin B‐complex) and control groups (antitubercular medicines). Data on adverse drug reactions and blood samples were collected at initiation, 2 months and 6 months, and then analyzed. Red blood cells and packed cell volume were significantly higher (P < 0.05) in the test group compared to control at 6 months of therapy. At the end of 2 months, results showed a significant decrease (P < 0.001) in aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, urea, creatinine and total bilirubin in the test group compared to control. Reduced glutathione and superoxide dismutase were significantly increased (P < 0.001) and malondialdehyde significantly decreased (P < 0.001) in the test versus control groups at the end of 2 and 6 months. Adverse drug reactions were significantly lower (P < 0.001) in the test group (32.4%) compared to control group (56.2%), with 1 death. Hepatotoxicity was significantly higher (P = 0.026) in control (6.9%), compared to test group (0%). Alcohol and cigarette smoking were significantly (P = 0.019 and P = 0.027) associated with the occurrence of adverse drug reactions. Methionine and vitamin B‐complex modulated hepatic, renal, hematological, antioxidant indices and adverse effects in patients administered antitubercular medicines. Such interventions can enhance compliance and better treatment outcomes in tuberculosis patients.

show abstract

Section: Discussioncontrasting

confidence: 77%

Methionine and vitamin B‐complex ameliorate antitubercular drugs‐induced toxicity in exposed patients

Amagon

Awodele

Akindele

2017

Pharmacology Res & Perspec

View full text Add to dashboard Cite

show abstract

“…Statistically speaking in 2017, there were more than 10 million reported cases of tuberculosis worldwide. The detection rate of ATLI ranges from 17.3% to 32.1% and varies in different countries, regions and amongst different races . The study found that the detection rate of ATLI in the process of standardized treatment of Mongolian tuberculosis patients was 27.6%.…”

Section: Discussionmentioning

confidence: 85%

“…Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis, which can usually invade one or more organs, lungs being the most common. According to the latest report from the World Health Organization in 2019, the number of tuberculosis patients in China is second only to India, and it is a country that carries a high burden of tuberculosis . Although the current anti‐tuberculosis drug treatment is gratifying, the adverse reactions in the course of treatment, such as liver injury caused by anti‐tuberculosis drugs (anti‐tuberculosis drug‐induced liver injury, ATLI), cannot be ignored.…”

Section: What Is Known and Objectivementioning

confidence: 99%

The role of NAT2 polymorphism and methylation in anti‐tuberculosis drug‐induced liver injury in Mongolian tuberculosis patients

et al. 2019

View full text Add to dashboard Cite

What is known and objective: Anti-tuberculosis drug-induced liver injury (ATLI) is one of the most significant adverse reactions for this line of therapy. N-acetyltransferase 2 (NAT2) is an important metabolic enzyme involved in drug metabolism and detoxification. Genetic polymorphism and DNA methylation have been proven to be key factors that affect the expression of NAT2. Therefore, the objective of the study was to investigate the relationship between NAT2 gene polymorphism and DNA methylation in the promoter region with ATLI risk in Mongolian tuberculosis patients. Methods:Our study is a case-control design. Chi-square test, Mann-Whitney U nonparametric test and Pearson test were all used to analyse existing relationships. The association between NAT2 gene acetylation phenotype and the total methylation of the NAT2 promoter region was analysed by means of binary logistic regression analysis. The general situation of the patients was evaluated by questionnaire, and the NAT2 genotyping of the three major polymorphism loci of gene coding was carried out by a gene sequencing technique. The methylation status of the NAT2 gene promoter region was detected by bisulphite sequencing and mass spectrometry.Result and discussion: Our study found that the detection rate of ATLI in Mongolian tuberculosis patients was 27.6%. There were no significant differences in demographic characteristics and living habits amongst the two groups, while significant differences were observed in the polymorphism of the NAT2 genes 481 (rs1799929) and 590 (rs1799930) and the acetylation phenotype. Moreover, the composition and distribution of the NAT2*4/4 and NAT2*4/5 genotypes were found in the two groups. The risk of ATLI in the slow acetylation type was 3.56 times higher than that of the fast acetylation type. Compared with the control group, the CpG5, CpG10, CpG11.12 and total methylation of the NAT2 promoter region in the ATLI group showed a hypermethylated pattern (P < .05). However, on performing binary logistic regression, neither the slow acetylation, intermediate acetylation nor rapid acetylation were found to be associated with ATLI (P > .05). It was found that the total methylation of NAT2 gene promoter region was an independent influencing factor of ATLI in Mongolian tuberculosis How to cite this article: Zhang D, Hao J, Hou R, Yu Y, Hu B, Wei L. The role of NAT2 polymorphism and methylation in anti-tuberculosis drug-induced liver injury in Mongolian tuberculosis patients. J Clin Pharm Ther. 2020;45:561-569.

show abstract

“…The proliferation of MDR TB leads to relapse and no single drug can treat them effectively. In 2014, 480,000 out of the 9.6 million people with TB infection were reported to have resistant TB variants [3]. In response to this challenge, clinical treatment standards suggested by the WHO require the use of a combination of anti-TB drugs to effectively control relapse [4].…”

Section: Introductionmentioning

confidence: 99%

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

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

View full text Add to dashboard Cite

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.

show abstract

Antituberculosis drugs and hepatotoxicity among hospitalized patients in Jos, Nigeria

Cited by 26 publications

References 16 publications

Methionine and vitamin B‐complex ameliorate antitubercular drugs‐induced toxicity in exposed patients

Methionine and vitamin B‐complex ameliorate antitubercular drugs‐induced toxicity in exposed patients

The role of NAT2 polymorphism and methylation in anti‐tuberculosis drug‐induced liver injury in Mongolian tuberculosis patients

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

Contact Info

Product

Resources

About