Evidence map›Paper›PMID 27283331›Full record

ArticleAnnals of the rheumatic diseases2017

Combined role of vitamin D status and CYP24A1 in the transition to systemic lupus erythematosus.

Kendra A Young, Melissa E Munroe, Joel M Guthridge, Diane L Kamen, Timothy B Niewold, Gary S Gilkeson, Michael H Weisman, Mariko L Ishimori, Jennifer Kelly, Patrick M Gaffney and 7 more

Open access · greenAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2017. 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
5.7field-weighted citation impact, top 4% 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, 49 citations in OpenAlex.

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  4. REDEFINING AUTOIMMUNE DISEASES: THE OPPORTUNITY FOR PRECISION AND PREVENTION.Transactions of the American Clinical and Climatological Association · 2025
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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

17 authors at 7 institutions in 1 country.

Kendra A YoungColorado School of Public Health, Aurora, Colorado, USA.
Melissa E MunroeOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.ORCID http://orcid.org/0000-0002-6933-9745
Joel M GuthridgeOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Diane L KamenMedical University of South Carolina, Charleston, South Carolina, USA.
Timothy B NiewoldMayo Clinic, Rochester, Minnesota, USA.ORCID http://orcid.org/0000-0003-3532-6660
Gary S GilkesonMedical University of South Carolina, Charleston, South Carolina, USA.
Michael H WeismanCedars-Sinai Medical Center, Los Angeles, California, USA.
Mariko L IshimoriCedars-Sinai Medical Center, Los Angeles, California, USA.
Jennifer KellyOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Patrick M GaffneyOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Kathy H SivilsOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Rufei LuOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Daniel J WallaceCedars-Sinai Medical Center, Los Angeles, California, USA.
David R KarpUniversity of Texas Southwestern Medical Center, Dallas, Texas, USA.
John B HarleyCincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Judith A JamesOklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Jill M NorrisColorado School of Public Health, Aurora, Colorado, USA.
Oklahoma Medical Research Foundation · USCedars-Sinai Medical Center · USColorado School of Public Health · USMedical University of South Carolina · USCincinnati Children's Hospital Medical Center · USMayo Clinic · USThe University of Texas Southwestern Medical Center · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI PAUL G SPICER · 2013 to 2026
$68.2M
SNP Confirmation and High Throughput Genotyping CoreP30AR053483 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GUTHRIDGE, JOEL MARVIN · 2007 to 2017
$6.7M
Pre-Clinical Studies to Identify SLE Therapeutic TargetsU19AI082714 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GAFFNEY, PATRICK M · 2009 to 2018
$6.2M
Patient Resource CoreP60AR062755 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SILVER, RICHARD M. · 2012 to 2016
$5.8M
Science in a Culture of MentoringP30GM103510 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2012 to 2016
$3.9M
Understanding early events in lupus autoimmunity to aid preventionU01AI101934 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2012 to 2016
$2.3M
NIAID NIH HHS U01 AI101934NIAID NIH HHS U19 AI082714NIAMS NIH HHS P30 AR053483NIAMS NIH HHS P60 AR062755NIGMS NIH HHS P30 GM103510NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

objectiveWe examined whether measures of vitamin D were associated with transitioning to systemic lupus erythematosus (SLE) in individuals at risk for SLE.

methods436 individuals who reported having a relative with SLE but who did not have SLE themselves were evaluated at baseline and again an average of 6.3 (±3.9) years later. Fifty-six individuals transitioned to SLE (≥4 cumulative American College of Rheumatology criteria). 25-Hydroxyvitamin D (25[OH]D) levels were measured by ELISA. Six single-nucleotide polymorphisms in four vitamin D genes were genotyped. Generalised estimating equations, adjusting for correlation within families, were used to test associations between the vitamin D variables and the outcome of transitioning to SLE.

resultsMean baseline 25[OH]D levels (p=0.42) and vitamin D supplementation (p=0.65) were not different between those who did and did not transition to SLE. Vitamin D deficiency (25[OH]D <20 ng/mL) was greater in those who transitioned compared with those who did not transition to SLE (46% vs 33%, p=0.05). The association between 25[OH]D and SLE was modified by CYP24A1 rs4809959, where for each additional minor allele increased 25[OH]D was associated with decreased SLE risk: zero minor alleles (adjusted OR: 1.03, CI 0.98 to 1.09), one minor allele (adjusted OR: 1.01, CI 0.97 to 1.05) and two minor alleles (adjusted OR: 0.91, CI 0.84 to 0.98). Similarly, vitamin D deficiency significantly increased the risk of transitioning to SLE in those with two minor alleles at rs4809959 (adjusted OR: 4.90, CI 1.33 to 18.04).

conclusionsVitamin D status and CYP24A1 may have a combined role in the transition to SLE in individuals at increased genetic risk for SLE.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseAdultAgedAllelesFemaleGenetic Predisposition to DiseaseHumansLongitudinal StudiesLupus Erythematosus, SystemicMaleMiddle AgedPolymorphism, Single NucleotideReceptors, CalcitriolRisk FactorsVitamin DVitamin D3 24-Hydroxylase1,25-dihydroxyvitamin D25-hydroxyvitamin D25-Hydroxyvitamin D3 1-alpha-HydroxylaseCYP24A1 protein, humanCYP27B1 protein, humanReceptors, CalcitriolVitamin DVitamin D3 24-HydroxylaseVitamin D-Binding ProteinEpidemiologyGene PolymorphismSystemic Lupus Erythematosus

Identifiers

PMID27283331
PMCPMC5360632
OpenAlexW2414857752

What OpenQuestion holds

Textmetadata
LicenceTDM
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.