Evidence map›Paper›PMID 23717666›Full record

Trial reportPloS one2013

Changes in airway histone deacetylase2 in smokers and COPD with inhaled corticosteroids: a randomized controlled trial.

Sukhwinder Singh Sohal, David Reid, Amir Soltani, Steven Weston, Hans Konrad Muller, Richard Wood-Baker, Eugene Haydn Walters

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Inhaled corticosteroid normalizes some but not all airway vascular remodeling in COPD.International journal of chronic obstructive pulmonary disease · 2016
    Trial
  3. Trial
  4. Trial
  5. Reply to BardsleyAmerican journal of respiratory and critical care medicine · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Fully integrating pathophysiological insights in COPD: an updated working disease model to broaden therapeutic vision.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  11. Article
  12. Review
  13. Review
  14. Inhaled corticosteroids for chronic obstructive pulmonary disease: what is their role in therapy?International journal of chronic obstructive pulmonary disease · 2018
    Review
  15. Article
  16. Article
  17. 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

7 authors at 1 institution in 1 country.

Sukhwinder Singh SohalBreathe Well Centre for Research Excellence in Chronic Respiratory Disease, University of Tasmania School of Medicine, Hobart, Australia. sssohal@utas.edu.au
David Reid
Amir Soltani
Steven Weston
Hans Konrad Muller
Richard Wood-Baker
Eugene Haydn Walters
University of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of HDAC2 is reported as reduced in chronic obstructive pulmonary disease (COPD). We assessed HDAC2 expression within the airways of smokers and subjects with COPD and effects of inhaled corticosteroids (ICS), using immuno-histology to contrast with previous molecular methodology. Endobronchial biopsies (ebb) from current smokers with COPD (COPD-CS; n = 15), ex-smokers with COPD (COPD-ES; n = 17), smokers with normal lung function (NS; n = 16) and normal controls (NC; n = 9) were immunostained for HDAC2. A double-blinded, randomized, placebo-controlled 6 months intervention study assessed effects of ICS on HDAC2 in 34 COPD subjects. There was no difference in epithelial HDAC2 staining in all groups. There was a significant reduction in total cell numbers in the lamina propria (LP) in COPD-CS and NS (p<0.05). LP cellularity correlated inversely with smoking history in COPD-CS (R = -0.8, p<0.003). HDAC2 expression increased markedly in NS (p<0.001); in contrast COPD-CS was associated with suppressed signal (p<0.03), while normal in COPD-ES. ICS did not affect HDAC2 cell staining. Our findings suggest that airway HDAC2 expression is increased in the LP by smoking itself, but is reduced in COPD. Ex-smokers have normalised HDAC2 cell expression, but ICS had no effect. The paper emphasise the pit-falls of relying on molecular data alone to define airway changes. CLINICAL TRIAL REGISTRATION INFORMATION: NAME OF REGISTRY: The Australian New Zealand Clinical Trials Registry (ANZCTR). REGISTRY NUMBER: ACTRN12612001111864.

Indexed as

SmokingAdministration, InhalationAgedBronchiBronchoscopyFemaleHistone Deacetylase 2HumansMaleMiddle AgedPulmonary Disease, Chronic ObstructiveHistone Deacetylase 2

Identifiers

PMID23717666
PMCPMC3661479
OpenAlexW1996262745

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.