Evidence map›Paper›PMID 22649569›Full record

ArticlePloS one2012

Impact of isoniazid resistance-conferring mutations on the clinical presentation of isoniazid monoresistant tuberculosis.

Raymund Dantes, John Metcalfe, Elizabeth Kim, Midori Kato-Maeda, Philip C Hopewell, Masae Kawamura, Payam Nahid, Adithya Cattamanchi

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Predicting isoniazid resistance inJournal of clinical microbiology · 2026
    Article
  2. Article
  3. Article
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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.

Raymund DantesDivision of Pulmonary and Critical Care Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, California, United States of America. raydantes@gmail.com
John Metcalfe
Elizabeth Kim
Midori Kato-Maeda
Philip C Hopewell
Masae Kawamura
Payam Nahid
Adithya Cattamanchi

Funding

POPULATION-BASED MOLECULAR EPIDEMIOLOGY OF TUBERCULOSISR01AI034238 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOPEWELL, PHILIP C · 1993 to 2010
$9.3M
Immunodiagnosis of Active Tuberculosis in HIV-infected PatientsK23HL094141 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CATTAMANCHI, ADITHYA · 2009 to 2013
$760k
Interplay of strain and ethnicity in the immune response to M. tuberculosisK23HL092629 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NAHID, PAYAM · 2007 to 2011
$626k
NHLBI NIH HHS K23 HL092629NHLBI NIH HHS K23HL092629NHLBI NIH HHS K23 HL094141NHLBI NIH HHS K23HL094141NIAID NIH HHS R01 AI034238NIAID NIH HHS R01AI034238
6 · The paper itself

Abstract

backgroundSpecific isoniazid (INH) resistance conferring mutations have been shown to impact the likelihood of tuberculosis (TB) transmission. However, their role in the clinical presentation and outcomes of TB has not been evaluated.

methodsWe included all cases of culture-confirmed, INH monoresistant tuberculosis reported to the San Francisco Department of Public Health Tuberculosis Control Section from October 1992 through October 2005. For cases with stored culture isolates, we used polymerase chain reaction (PCR) testing and gene sequencing to identify INH resistance-conferring mutations, and compared genotypic and phenotypic characteristics.

resultsAmong 101 consecutive cases of INH monoresistant TB in San Francisco 19 (19%) had isolates with a katG mutation other than S315T; 38 (38%) had isolates with the katG S315T mutation, 29 (29%) had isolates with a inhA-15;c-t promoter mutation, and 15 (15%) had isolates with other mutations. The katG S315T mutation was independently associated with high-level INH resistance (risk ratio [RR] 1.56, 95% confidence interval [CI] 1.07-2.27), and the inhA-15;c-t promoter mutation was inversely associated with high-level INH resistance (RR 0.43, 95% CI 0.21-0.89). However, specific INH resistance-conferring mutations were not associated with the clinical severity or outcomes of INH monoresistant TB cases.

conclusionThese data suggest that INH resistance-conferring mutations do not impact the clinical presentation of TB.

Indexed as

IsoniazidBacterial ProteinsCatalaseDrug ResistanceGenotypeHumansMycobacterium tuberculosisOxidoreductasesReal-Time Polymerase Chain ReactionRetrospective StudiesSan FranciscoSequence Analysis, DNASpecies SpecificityStatistics, NonparametricTuberculosisBacterial ProteinsCatalaseInhA protein, MycobacteriumIsoniazidkatG protein, Mycobacterium tuberculosisOxidoreductases

Identifiers

PMID22649569
PMCPMC3359338

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Registered trials

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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.