Evidence map›Paper›PMID 14694251›Full record

ArticleThorax2004

Low birth weight for gestation and airway function in infancy: exploring the fetal origins hypothesis.

C Dezateux, S Lum, A-F Hoo, J Hawdon, K Costeloe, J Stocks

Open access · greenAbstract read
In one paragraph

Article in Thorax, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 105 citations in OpenAlex.

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  14. Observational
  15. Maternal protein restriction alters VEGF signaling and decreases pulmonary alveolar in fetal rats.International journal of clinical and experimental pathology · 2014
    Article
  16. Review
  17. Article
  18. Fetal growth and risk of childhood asthma and allergic disease.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2012
    Review
  19. Article
  20. 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

6 authors.

C DezateuxCentre for Paediatric Epidemiology and Biostatistics, Institute of Child Health, London, UK. c.dezateux@ich.ucl.ac.uk
S Lum
A-F Hoo
J Hawdon
K Costeloe
J Stocks

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPoor fetal growth has been associated with impaired airway function in adult life, but evidence linking birth weight and airway function in early childhood is sparse. We examined the hypothesis that low birth weight for gestation is associated with impaired airway function shortly after birth and that this is independent of impaired postnatal somatic growth.

methodsAirway function was measured using the raised volume technique in healthy white infants of low (< or =10th centile) or appropriate (> or =20th centile) birth weight for gestation and was expressed as forced expiratory volume in 0.4 s (FEV0.4), forced vital capacity (FVC), and the maximal expired flow at 25% of forced vital capacity (MEF25). Infant length and weight, maternal height and weight, maternal report of smoking prenatally and postnatally, and parental occupation were recorded.

resultsMothers of low birth weight for gestation infants (n=98) were lighter, shorter, and more likely to smoke and have partners in manual occupations. At 6 weeks their infants remained lighter and shorter than those of appropriate birth weight (n=136). FEV0.4, FVC, and MEF25 were reduced in infants of low birth weight for gestation, in those whose mothers smoked in pregnancy, or who were in manual occupations. After adjusting for relevant maternal and infant characteristics, infants in the low birth weight for gestation group experienced a mean reduction of 11 ml in FEV0.4 (95% CI 4 to 18; p=0.002), of 12 ml in FVC (95% CI 4 to 19; p=0.004), and of 28 ml/s in MEF25 (95% CI 7 to 48; p=0.03).

conclusionsAirway function is diminished in early postnatal life as a consequence of a complex causal pathway which includes social disadvantage as indicated by maternal social class, smoking and height, birth weight as a proximal and related consequence of these factors, and genetic predisposition to asthma. Further work is needed to establish the relevance of these findings to subsequent airway growth and development in later infancy and early childhood.

Indexed as

Bronchial DiseasesFemaleFetal Growth RetardationForced Expiratory VolumeGestational AgeHumansInfant, Low Birth WeightInfant, NewbornMaleMaximal Midexpiratory Flow RateMultivariate AnalysisProspective StudiesVital Capacity

Identifiers

PMID14694251
PMCPMC1758850
OpenAlexW2098979540

What OpenQuestion holds

Textmetadata
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.