Evidence map›Paper›PMID 26259119›Full record

ArticleJournal of hypertension2015

Refined phenotyping identifies links between preeclampsia and related diseases in a Norwegian preeclampsia family cohort.

Liv Cecilie V Thomsen, Phillip E Melton, Kjersti Tollaksen, Ingvill Lyslo, Linda T Roten, Maria L Odland, Kristin M Strand, Ottar Nygård, Chen Sun, Ann-Charlotte Iversen and 3 more

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In one paragraph

Article in Journal of hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.4field-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.

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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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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

13 authors at 5 institutions in 3 countries.

Liv Cecilie V ThomsenaDepartment of Gynecology and Obstetrics, Haukeland University Hospital bDepartment of Clinical Science, University of Bergen, Bergen, Norway cCentre for Genetic Origins of Health and Disease, University of Western Australia, Perth, Australia dCentre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim eDepartment of Obstetrics and Gynecology, Stavanger University Hospital, Stavanger fDepartment of Cancer Research and Molecular Medicine gDepartment of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim hDepartment of Heart Disease, Haukeland University Hospital, Bergen, Norway.
Phillip E Melton
Kjersti Tollaksen
Ingvill Lyslo
Linda T Roten
Maria L Odland
Kristin M Strand
Ottar Nygård
Chen Sun
Ann-Charlotte Iversen
Rigmor Austgulen
Eric K Moses
Line Bjørge
Haukeland University Hospital · NONorwegian University of Science and Technology · NOStavanger University Hospital · NOUniversity of Western Australia · AUGTx (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePreeclampsia is a complex genetic disease of pregnancy with a heterogenous presentation, unknown cause and potential severe outcomes for both mother and child. Preeclamptic women have increased risk for atherothrombotic cardiovascular disease. We aimed to identify heritabilities and phenotypic correlations of preeclampsia and related conditions in the Norwegian Preeclampsia Family Biobank.

methodsBy applying a variance components model, a total of 493 individuals (from 138 families with increased occurrence of preeclampsia) were classified according to 30 disease-related phenotypes.

resultsOf parous women, 75.7% (263/338) had experienced preeclampsia and 35.7% of women with and 22.4% without preeclampsia delivered children small for gestational age (SGA). We identified 11 phenotypes as heritable. The increased occurrence of preeclampsia was reflected by the presence [heritability (H2r) = 0.60)] and severity (H2r = 0.15) of preeclampsia and being born in a preeclamptic pregnancy (H2r = 0.25). Other heritable phenotypes identified included SGA (H2r = 0.40), chronic hypertension (H2r = 0.57), severity of atherothrombotic cardiovascular disease (H2r = 0.31), BMI (H2r = 0.60) and pulmonary disease (H2r = 0.91). The heritable phenotype preeclampsia overlapped with SGA (P = 0.03), whereas pulmonary disease was phenotypically correlated with atherothrombotic cardiovascular disease (P < 0.01), SGA (P = 0.02) and BMI (P = 0.02).

conclusionThis is the first study identifying the H2r of a range of health-related conditions in preeclamptic families. Our study demonstrates how refinement of phenotypes leads to better H2r estimation and the identification of a biological relationship between preeclampsia and related traits.

Indexed as

Infant, Small for Gestational AgeAdultBiological Specimen BanksFemaleHumansInfant, NewbornMaleMothersNorwayPhenotypePre-EclampsiaPregnancy

Identifiers

PMID26259119
PMCPMC4596487
OpenAlexW1121571213

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.