ArticleMolecular biology reports2024
Exploring gene mutations and multidrug resistance in Mycobacterium tuberculosis: a study from the Lung Hospital in Vietnam.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Analysis of High-Risk Factors for Tuberculosis Retreatment Based on Machine Learning and Latent Class Analysis.Infection and drug resistance · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundDrug-resistant tuberculosis not only diminishes treatment efficacy but also heightens the risk of transmission and mortality. Investigating Mycobacterium tuberculosis resistance to first-line antituberculosis drugs is essential to tackle a major global health challenge. METHODS AND
resultsUsing Sanger sequencing, this study investigates gene mutations associated with multidrug resistance in drug-resistant M. tuberculosis strains. Among 30 samples, mutations were found in genes linked to first-line anti-tuberculosis drug resistance. Rifampicin resistance was observed in 46.67% of the samples, with the most frequent mutation in the rpoB gene at codon 450 (S450L) occurring in 23.33% of cases. Similarly, isoniazid resistance was found in 86.67% of samples, with 33.33% of cases indicating the katG gene mutation at codon 315 (S315T). Additionally, streptomycin resistance was present in 76.67% of samples, and 30% of these cases were mainly linked to the rpsL gene mutation at codon 43 (K43R).
conclusionThese findings illuminate the genetic mechanisms behind drug resistance in M. tuberculosis. By identifying specific genetic markers, this research enhances our ability to diagnose and treat drug-resistant Tuberculosis more accurately and efficiently.
Indexed as
Identifiers
39432118What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.