Evidence map›Paper›PMID 29161409›Full record

ArticleThe Journal of clinical endocrinology and metabolism2018

Transfer and Metabolism of Cortisol by the Isolated Perfused Human Placenta.

Laura I Stirrat, Bram G Sengers, Jane E Norman, Natalie Z M Homer, Ruth Andrew, Rohan M Lewis, Rebecca M Reynolds

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
15.8field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 95 citations in OpenAlex.

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  8. Models of Endocrine-Disrupting Effects: Human Placental Steroidogenesis.Basic & clinical pharmacology & toxicology · 2025
    Review
  9. Review
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  14. Placental transfer of tofacitinib in theCurrent research in toxicology · 2024
    Article
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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 3 institutions in 1 country.

Laura I StirratTommy's Centre for Maternal and Fetal Health, MRC Centre for Reproductive Health, University of Edinburgh, Edinburgh, United Kingdom.
Bram G SengersBioengineering Science Research Group, Faculty of Engineering and the Environment, University of Southampton, Southampton, United Kingdom.
Jane E NormanTommy's Centre for Maternal and Fetal Health, MRC Centre for Reproductive Health, University of Edinburgh, Edinburgh, United Kingdom.
Natalie Z M HomerMass Spectrometry Core, Edinburgh Clinical Research Facility, University of Edinburgh, Edinburgh, United Kingdom.
Ruth AndrewMass Spectrometry Core, Edinburgh Clinical Research Facility, University of Edinburgh, Edinburgh, United Kingdom.
Rohan M LewisInstitute for Life Sciences, University of Southampton, Southampton, United Kingdom.
Rebecca M ReynoldsTommy's Centre for Maternal and Fetal Health, MRC Centre for Reproductive Health, University of Edinburgh, Edinburgh, United Kingdom.
MRC Centre for Reproductive Health · GBUniversity of Edinburgh · GBUniversity of Southampton · GB

Funding

British Heart FoundationMedical Research Council MR/N022556/1
6 · The paper itself

Abstract

Context: Fetal overexposure to glucocorticoids in utero is associated with fetal growth restriction and is postulated to be a key mechanism linking suboptimal fetal growth with cardiovascular disease in later life. Objective: To develop a model to predict maternal-fetal glucocorticoid transfer. We hypothesized placental 11-β-hydroxysteroid dehydrogenase-type 2 (11β-HSD2) would be the major rate-limiting step in maternal cortisol transfer to the fetus. Design: We used a deuterated cortisol tracer in the ex vivo placental perfusion model, in combination with computational modeling, to investigate the role of interconversion of cortisol and its inactive metabolite cortisone on transfer of cortisol from mother to fetus. Participants: Term placentas were collected from five women with uncomplicated pregnancies, at elective caesarean delivery. Intervention: Maternal artery of the isolated perfused placenta was perfused with D4-cortisol. Main Outcome Measures: D4-cortisol, D3-cortisone, and D3-cortisol were measured in maternal and fetal venous outflows. Results: D4-cortisol, D3-cortisone, and D3-cortisol were detected and increased in maternal and fetal veins as the concentration of D4-cortisol perfusion increased. D3-cortisone synthesis was inhibited when 11-β-hydroxysteroid dehydrogenase (11β-HSD) activity was inhibited. At the highest inlet concentration, only 3.0% of the maternal cortisol was transferred to the fetal circulation, whereas 26.5% was metabolized and 70.5% exited via the maternal vein. Inhibiting 11β-HSD activity increased the transfer to the fetus to 7.3% of the maternal input, whereas 92.7% exited via the maternal vein. Conclusions: Our findings challenge the concept that maternal cortisol diffuses freely across the placenta and confirm that 11β-HSD2 acts as a major "barrier" to cortisol transfer to the fetus.

Indexed as

AdultBiological TransportBirth WeightFemaleHumansHydrocortisoneInfant, NewbornMaternal-Fetal RelationsOrgan Culture TechniquesPerfusionPlacentaPlacental CirculationPregnancyPregnancy Trimester, ThirdStress, PsychologicalHydrocortisone

Identifiers

PMID29161409
PMCPMC5800837
OpenAlexW2770217230

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.