Evidence map›Paper›PMID 21494147›Full record

ReviewCurrent opinion in pediatrics2011

Pathogenesis and treatment of bronchopulmonary dysplasia.

Jason Gien, John P Kinsella

2 registry-linked trialsAbstract readReview
In one paragraph

Review in Current opinion in pediatrics, 2011. 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 77 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 4 pooled it
9.7field-weighted citation impact, top 2% 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.

NCT01721655 phase2 / phase3unknown statusnot on this mapstarted 2012, after this paper: background citation

Determining the Effect of Spironolactone on Electrolyte Supplementation in Preterm Infants With Chronic Lung Disease

TypeinterventionalSponsorWest Virginia University HealthcareRan2012 to 2016Enrolled40ConditionsChronic Lung Disease, Bronchopulmonary DysplasiaArmsSpironolactone, Placebo
NCT02147457 completednot on this mapstarted 2014, after this paper: background citation

Prematurity as Predictor of Children's Cardiovascular-renal Health (PREMATCH)

TypeobservationalSponsorUniversitaire Ziekenhuizen KU LeuvenRan2014 to 2015Enrolled180ConditionsEndothelial Dysfunction, Sublingual Capillary Glycocalyx and Density, Visual Disturbances and Blindness, Ventricular Dysfunction, Left
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 4 syntheses or guidelines pooled it, 169 citations in OpenAlex.

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  5. Ancestry and genetic associations with bronchopulmonary dysplasia in preterm infants.American journal of physiology. Lung cellular and molecular physiology · 2018
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17 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Jason GienThe Pediatric Heart Lung Center, Section of Neonatology, University of Colorado School of Medicine, Aurora, USA. jason.gien@ucdenver.edu
John P Kinsella
University of Colorado Denver · US

Funding

Rho-kinase signaling in lung development and persistent pulmonary hypertensionK08HL102261 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GIEN, JASON · 2010 to 2014
$662k
NHLBI NIH HHS 1K08HL102261NHLBI NIH HHS K08 HL102261
6 · The paper itself

Abstract

purpose of reviewBronchopulmonary dysplasia (BPD) is a chronic lung disease of infancy affecting mostly premature infants with significant morbidity and mortality. Improved survival of very immature infants has led to increased numbers of infants with this disorder. Acute and chronic lung injury and impaired postnatal lung growth are thought to be responsible for the development of BPD. Whereas changes in clinical practice have improved the clinical course and outcomes for infants with BPD, over the past decade, the overall incidence of BPD has not changed. This review will describe the prenatal and postnatal factors that contribute to the pathogenesis of BPD as well as current and experimental therapies for treatment of BPD. RECENT

findingsThe factors that contribute to the pathogenesis of BPD are well described; however, recent studies have better defined how these factors modulate lung growth. Inflammation, proinflammatory cytokines and altered angiogenic gene signaling contribute to lung injury and impair prenatal and postnatal lung growth resulting in BPD; however, to date no therapy has been identified that potently and consistently prevents or reverses their effects on lung growth. We will discuss the cell signaling pathways affected in BPD and current therapies available for modulating these pathways. SUMMARY: Despite current advances in neonatal care, BPD remains a heavy burden on healthcare resources. New treatments directed at either reducing lung injury or improving lung growth are under study.

Indexed as

Adrenal Cortex HormonesBronchopulmonary DysplasiaHumansInfant, NewbornInfant, PrematureTransforming Growth Factor beta1Vascular Endothelial Growth Factor AAdrenal Cortex HormonesTransforming Growth Factor beta1Vascular Endothelial Growth Factor A

Identifiers

PMID21494147
PMCPMC3767848
OpenAlexW2072037443

What OpenQuestion holds

Textmetadata
LicenceTDM
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.