Evidence map›Paper›PMID 31324189›Full record

Trial reportRespiratory research2019

DSP variants may be associated with longitudinal change in quantitative emphysema.

Woori Kim, Michael H Cho, Phuwanat Sakornsakolpat, David A Lynch, Harvey O Coxson, Ruth Tal-Singer, Edwin K Silverman, Terri H Beaty

2 registry-linked trialsOpen access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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.

NCT00292552 completednot on this map

A Multicentre 3 Year Longitudinal Prospective Study to Identify Novel Endpoints and Compare These With Forced Expiratory Volume in 1 Second (FEV1) for Their Ability to Measure and Predict COPD Severity and Its Progression Over Time

TypeobservationalSponsorGlaxoSmithKlineRan2005 to 2010Enrolled2,747ConditionsPulmonary Disease, Chronic ObstructiveArmsNovel endpoint determination
NCT00608764 active not recruitingnot on this map

Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene)

TypeobservationalSponsorBrigham and Women's HospitalRan2007 to 2028Enrolled10,718ConditionsPulmonary Disease, Chronic Obstructive, Emphysema, Bronchitis, Chronic
3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Frontiers in physiology · 2021
    Article
  8. Differential Genomic Profile inFrontiers in medicine · 2021
    Article
  9. Desmoplakin: An Important Player in Aging Lung Disease.American journal of respiratory and critical care medicine · 2020
    Article
  10. Therapeutic advances in respiratory disease
    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 5 institutions in 3 countries.

Woori KimDepartment of Epidemiology, Johns Hopkins School of Public Health, 615 N. Wolfe Street, Baltimore, MD, 21205, USA.
Michael H ChoChanning Division of Network Medicine Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Phuwanat SakornsakolpatChanning Division of Network Medicine Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
David A LynchDepartment of Radiology, National Jewish Health, Denver, CO, USA.
Harvey O CoxsonDepartment of Radiology, University of British Columbia, British Columbia, Canada.
Ruth Tal-SingerGSK, Collegeville, PA, USA.
Edwin K SilvermanChanning Division of Network Medicine Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Terri H BeatyDepartment of Epidemiology, Johns Hopkins School of Public Health, 615 N. Wolfe Street, Baltimore, MD, 21205, USA. tbeaty1@jhu.edu.ORCID http://orcid.org/0000-0002-7644-1705
Brigham and Women's Hospital · USGlaxoSmithKline (United States) · USJohns Hopkins University · USNational Jewish Health · USUniversity of British Columbia · CA

Funding

Genetic Epidemiology of COPDU01HL089897 · NHLBI · NATIONAL JEWISH HEALTH · PI CRAPO, JAMES D · 2007 to 2021
$56.9M
Genetic Epidemiology of COPDU01HL089856 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SILVERMAN, EDWIN K · 2007 to 2021
$20.7M
GlaxoSmithKline NCT00292552NHLBI NIH HHS U01 HL089856NHLBI NIH HHS U01 HL089897
6 · The paper itself

Abstract

backgroundEmphysema, characterized by lung destruction, is a key component of Chronic Obstructive Pulmonary Disease (COPD) and is associated with increased morbidity and mortality. Genome-wide association studies (GWAS) have identified multiple genetic factors associated with cross-sectional measures of quantitative emphysema, but the genetic determinants of longitudinal change in quantitative measures of emphysema remain largely unknown. Our study aims to identify genetic variants associated with longitudinal change in quantitative emphysema measured by computed tomography (CT) imaging.

methodsWe included current and ex-smokers from two longitudinal cohorts: COPDGene, a study of Non-Hispanic Whites (NHW) and African Americans (AA), and the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE). We calculated annual change in two quantitative measures of emphysema based on chest CT imaging: percent low attenuation area (≤ - 950HU) (%LAA-950) and adjusted lung density (ALD). We conducted GWAS, separately in 3030 NHW and 1158 AA from COPDGene and 1397 Whites from ECLIPSE. We further explored effects of 360 previously reported variants and a lung function based polygenic risk score on annual change in quantitative emphysema.

resultsIn the genome-wide association analysis, no variants achieved genome-wide significance (P < 5e-08). However, in the candidate region analysis, rs2076295 in the DSP gene, previously associated with COPD, lung function and idiopathic pulmonary fibrosis, was associated with change in %LAA-950 (β (SE) = 0.09 (0.02), P = 3.79e-05) and in ALD (β (SE) = - 0.06 (0.02), P = 2.88e-03). A lung function based polygenic risk score was associated with annual change in %LAA-950 (P = 4.03e-02) and with baseline measures of quantitative emphysema (P < 1e-03) and showed a trend toward association with annual change in ALD (P = 7.31e-02).

conclusionsDSP variants may be associated with longitudinal change in quantitative emphysema. Additional investigation of the DSP gene are likely to provide further insights into the disease progression in emphysema and COPD.

trial registrationClinicaltrials.gov Identifier: NCT00608764 , NCT00292552 .

Indexed as

Disease ProgressionAgedAged, 80 and overCohort StudiesDesmoplakinsFemaleFollow-Up StudiesGenetic Association StudiesGenetic VariationHumansLongitudinal StudiesMaleMiddle AgedPulmonary EmphysemaDesmoplakinsDSP protein, humanCOPDEmphysemaEmphysema progressionGeneticsGWAS

Identifiers

PMID31324189
PMCPMC6642569
OpenAlexW2964051463

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.