Evidence map›Paper›PMID 32002554›Full record

Observational studyThe Journal of infectious diseases2020

Isoniazid and Rifampin-Resistance Mutations Associated With Resistance to Second-Line Drugs and With Sputum Culture Conversion.

Eleanor S Click, Ekaterina V Kurbatova, Heather Alexander, Tracy L Dalton, Michael P Chen, James E Posey, Julia Ershova, J Peter Cegielski

Open access · bronzeAbstract readMulticenter StudyObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in The Journal of infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 30% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Precision Medicine Strategies to Improve Isoniazid Therapy in Patients with Tuberculosis.European journal of drug metabolism and pharmacokinetics · 2024
    Review
  4. Article
  5. Analysis of drug resistance and mutation profiles inThe Journal of international medical research · 2021
    Article
  6. Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Eleanor S ClickDivision of Global HIV and TB, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Ekaterina V KurbatovaDivision of Tuberculosis Elimination, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Heather AlexanderDivision of Global HIV and TB, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Tracy L DaltonDivision of Tuberculosis Elimination, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Michael P ChenDivision of Tuberculosis Elimination, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
James E PoseyDivision of Tuberculosis Elimination, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Julia ErshovaDivision of Global HIV and TB, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
J Peter CegielskiDivision of Global HIV and TB, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Centers for Disease Control and Prevention · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutations in the genes inhA, katG, and rpoB confer resistance to anti-tuberculosis (TB) drugs isoniazid and rifampin. We questioned whether specific mutations in these genes were associated with different clinical and microbiological characteristics.

methodsIn a multicountry prospective cohort study of multidrug-resistant TB, we identified inhA, katG, and rpoB mutations in sputum isolates using the Hain MTBDRplus line probe assay. For specific mutations, we performed bivariate analysis to determine relative risk of baseline or acquired resistance to other TB drugs. We compared time to sputum culture conversion (TSCC) using Kaplan-Meier curves and stratified Cox regression.

resultsIn total, 447 participants enrolled from January 2005 to December 2008 from 7 countries were included. Relative to rpoB S531L, isolates with rpoB D516V had less cross-resistance to rifabutin, increased baseline resistance to other drugs, and increased acquired fluoroquinolone resistance. Relative to mutation of katG only, mutation of inhA promoter and katG was associated with baseline extensively drug resistant (XDR) TB, increased acquired fluoroquinolone resistance, and slower TSCC (125.5 vs 89.0 days).

conclusionsSpecific mutations in inhA and katG are associated with differences in resistance to other drugs and TSCC. Molecular testing may make it possible to tailor treatment and assess additional drug resistance risk according to specific mutation profile.

Indexed as

Antitubercular AgentsBacterial ProteinsCatalaseDNA, BacterialDNA-Directed RNA PolymerasesDNA Mutational AnalysisDrug Resistance, Multiple, BacterialGenes, BacterialHumansIsoniazidMicrobial Sensitivity TestsMutationMycobacterium tuberculosisOxidoreductasesPromoter Regions, GeneticProspective StudiesAntitubercular AgentsBacterial ProteinsCatalaseDNA, BacterialDNA-Directed RNA PolymerasesInhA protein, MycobacteriumIsoniazidkatG protein, Mycobacterium tuberculosisOxidoreductasesRifampinrpoB protein, Mycobacterium tuberculosisculture conversiondrug resistanceisoniazidrifampinsecond-line drugs tuberculosis

Identifiers

PMID32002554
PMCPMC7289556
OpenAlexW3003630821

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.