oru.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Small for gestational age and risk of childhood mortality: A Swedish population study
Örebro University, School of Medical Sciences. Örebro University Hospital. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Orebro Univ Hosp, Dept Pediat, Orebro, Sweden.;Univ Nottingham, Div Epidemiol & Publ Hlth, Sch Med, Nottingham, England.;Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA..ORCID iD: 0000-0003-1024-5602
Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Univ Iceland, Fac Med, Ctr Publ Hlth Sci, Reykjavik, Iceland..
Karolinska Inst, Dept Lab Med, Clin Epidemiol Unit, Stockholm, Sweden..
Karolinska Inst, Dept Med, Stockholm, Sweden..
Show others and affiliations
2018 (English)In: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 15, no 12, article id e1002717Article in journal (Refereed) Published
Abstract [en]

Background: Small for gestational age (SGA) has been associated with increased risks of stillbirth and neonatal mortality, but data on long-term childhood mortality are scarce. Maternal antenatal care, including globally reducing the risk of SGA birth, may be key to achieving the Millennium Development Goal of reducing under-5 mortality. We therefore aimed to examine the association between SGA and mortality from 28 days to <18 years using a population-based and a sibling control design.

Methods and findings: In a Swedish population study, we identified 3,795,603 non-malformed singleton live births and 2,781,464 full siblings born from January 1, 1973, to December 31, 2012. We examined the associations of severe (<3rd percentile) and moderate (3rd to <10th percentile) SGA with risks of death from 28 days to <18 years after birth. Children born SGA were first compared to non-SGA children from the population, and then to non-SGA siblings. The sibling-based analysis, by design, features a better control for unmeasured factors that are shared between siblings (e.g., socioeconomic status, lifestyle, and genetic factors). Hazard ratios (HRs) were calculated using Cox proportional hazards and flexible parametric survival models. During follow-up (1973-2013), there were 10,838 deaths in the population-based analysis and 1,572 deaths in sibling pairs with discordant SGA and mortality status. The crude mortality rate per 10,000 person-years was 5.32 in children born with severe SGA, 2.76 in children born with moderate SGA, and 1.93 in non-SGA children. Compared with non-SGA children, children born with severe SGA had an increased risk of death in both the population-based (HR = 2.58, 95% CI = 2.38-2.80) and sibling-based (HR = 2.61, 95% CI = 2.19-3.10) analyses. Similar but weaker associations were found for moderate SGA in the population-based (HR = 1.37, 95% CI = 1.28-1.47) and sibling-based (HR = 1.38, 95% CI = 1.22-1.56) analyses. The excess risk was most pronounced between 28 days and <1 year of age but remained throughout childhood. The greatest risk increase associated with severe SGA was noted for deaths due to infection and neurologic disease. Although we have, to our knowledge, the largest study sample so far addressing the research question, some subgroup analyses, especially the analysis of cause-specific mortality, had limited statistical power using the sibling-based approach.

Conclusions: We found that SGA, especially severe SGA, was associated with an increased risk of childhood death beyond the neonatal period, with the highest risk estimates for death from infection and neurologic disease. The similar results obtained between the population- and sibling-based analyses argue against strong confounding by factors shared within families.

Place, publisher, year, edition, pages
Public Library of Science , 2018. Vol. 15, no 12, article id e1002717
National Category
Pediatrics
Identifiers
URN: urn:nbn:se:oru:diva-71542DOI: 10.1371/journal.pmed.1002717ISI: 000454833300008PubMedID: 30562348Scopus ID: 2-s2.0-85058870436OAI: oai:DiVA.org:oru-71542DiVA, id: diva2:1279900
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2017-00134
Note

Funding Agency:

Karolinska Institutet

Available from: 2019-01-17 Created: 2019-01-17 Last updated: 2019-01-17Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records BETA

Ludvigsson, Jonas F.

Search in DiVA

By author/editor
Ludvigsson, Jonas F.
By organisation
School of Medical SciencesÖrebro University Hospital
In the same journal
PLoS Medicine
Pediatrics

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 52 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf