Evidence map›Paper›PMID 42532549›Full record

ArticleRMD open2026

Maternal weight and hypertension as risk factors for juvenile idiopathic arthritis: a prospective population-based pregnancy cohort study.

Vilde Øverlien Dåstøl, Ida Henriette Caspersen, Kristine Løkås Haftorn, Sigrid Valen Hestetun, Srijana Bastakoti, Ole Andreassen, Anne Lise Brantsæter, Siri Eldevik Håberg, Karen H Costenbader, Ketil Størdal and 1 more

Abstract read
In one paragraph

Article in RMD open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Vilde Øverlien Dåstøl *Department of Rheumatology, Oslo University Hospital, Oslo, Norway vilde.dastol@gmail.com.ORCID http://orcid.org/0009-0000-6156-4350
Ida Henriette Caspersen *Department of Rheumatology, Oslo University Hospital, Oslo, Norway.
Kristine Løkås HaftornDepartment of Rheumatology, Oslo University Hospital, Oslo, Norway.
Sigrid Valen HestetunDepartment of Rheumatology, Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0009-0004-4199-4950
Srijana BastakotiDepartment of Rheumatology, Oslo University Hospital, Oslo, Norway.
Ole AndreassenKG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo and Oslo University Hospital, Oslo, Norway.
Anne Lise BrantsæterNorwegian Institute of Public Health, Centre for Sustainable Diets, Oslo, Norway.ORCID http://orcid.org/0000-0001-6315-7134
Siri Eldevik HåbergCentre for Fertility and Health, Norwegian Institute of Public Health, Oslo, Norway.
Karen H CostenbaderDepartment of Medicine, Division of Rheumatology, Inflammation and Immunity, Brigham and Women's Hospital, Boston, Massachusetts, USA.ORCID http://orcid.org/0000-0002-8972-9388
Ketil StørdalDepartment of Pediatric Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Helga SannerDepartment of Rheumatology, Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0000-0001-7226-066X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe intrauterine environment may influence childhood immune-mediated disease risk. We investigated whether maternal prepregnancy body mass index (BMI), gestational weight gain (GWG) or hypertensive disorders during pregnancy (HDP) were associated with juvenile idiopathic arthritis (JIA) in children and whether genetic susceptibility modified associations.

methodsWe linked the Norwegian Mother, Father and Child Cohort Study (MoBa) to the Norwegian Patient Registry to identify children with JIA. Logistic regression estimated adjusted ORs (aORs) for associations with BMI, GWG and HDPs. Causal mediation analyses assessed whether hypertension mediated the GWG-JIA association. In a genotyped subsample, we tested interactions between exposures and a JIA Polygenic Risk Score (PRS).

resultsAmong 78 901 eligible children, 265 developed JIA (genotyped subsample: 192 JIA/44 053 non-JIA). By the end of follow-up, all children were ≥14 years old and 85% were ≥16 years old. Maternal prepregnancy BMI was not associated with JIA. Each 1 SD (~6 kg) increase in GWG was associated with modestly higher odds of JIA (aOR 1.12, 95% CI 1.00 to 1.26), particularly among women with prepregnancy obesity (aOR 1.40, 95% CI 1.10 to 1.77). Maternal hypertension and pre-eclampsia were associated with higher JIA risk (aOR 1.43, 95% CI 1.02 to 1.99 and aOR 1.61, 95% CI 1.10 to 2.37). Hypertension did not mediate the GWG-JIA association (p>0.05). Among children with lower PRS, maternal obesity was associated with a lower JIA risk (aOR 0.37, 95% CI 0.17 to 0.80).

conclusionHigher GWG and HDPs were independently associated with increased JIA risk. Genetic susceptibility may modify associations with maternal BMI, supporting a role for pregnancy health in JIA development.

Indexed as

Arthritis, JuvenileBody WeightHypertensionPrenatal Exposure Delayed EffectsAdolescentAdultBody Mass IndexChildFemaleGenetic Predisposition to DiseaseGenetic Risk ScoreGestational Weight GainHumansHypertension, Pregnancy-InducedMaleNorwayEpidemiologyHypertensionInflammationJuvenile Idiopathic ArthritisPublic Health

Identifiers

PMID42532549
PMCPMC13435918

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.