Evidence map›Paper›PMID 27467283›Full record

ArticleGenes and immunity2016

Genetic risk and longitudinal disease activity in systemic lupus erythematosus using targeted maximum likelihood estimation.

M A Gianfrancesco, L Balzer, K E Taylor, L Trupin, J Nititham, M F Seldin, A W Singer, L A Criswell, L F Barcellos

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

9 authors.

M A GianfrancescoDivision of Epidemiology, University of California, Berkeley, CA, USA.
L BalzerDivision of Biostatistics, University of California, Berkeley, CA, USA.
K E TaylorDepartment of Medicine, Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, CA, USA.
L TrupinDepartment of Medicine, Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, CA, USA.
J NitithamDepartment of Medicine, Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, CA, USA.
M F SeldinDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
A W SingerDivision of Epidemiology, University of California, Berkeley, CA, USA.
L A CriswellDepartment of Medicine, Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, University of California, San Francisco, CA, USA.
L F BarcellosDivision of Epidemiology, University of California, Berkeley, CA, USA.

Funding

Engaging University of California Stakeholders for Biorespository ResearchUL1TR000004 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRANDIS, JENNIFER RUBIN · 2012 to 2015
$78.0M
The Interplay of Sociodemographic and Genetic Factors in SLE Health DisparitiesP60AR053308 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YELIN, EDWARD H · 2006 to 2016
$11.8M
The Genetic Epidemiology of RA and SLEK24AR002175 · NIAMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CRISWELL, LINDSEY ANN · 2001 to 2005
$555k
NCATS NIH HHS UL1 TR000004NIAMS NIH HHS K24 AR002175NIAMS NIH HHS P60 AR053308
6 · The paper itself

Abstract

Systemic lupus erythematous (SLE) is a chronic autoimmune disease associated with genetic and environmental risk factors. However, the extent to which genetic risk is causally associated with disease activity is unknown. We utilized longitudinal-targeted maximum likelihood estimation to estimate the causal association between a genetic risk score (GRS) comprising 41 established SLE variants and clinically important disease activity as measured by the validated Systemic Lupus Activity Questionnaire (SLAQ) in a multiethnic cohort of 942 individuals with SLE. We did not find evidence of a clinically important SLAQ score difference (>4.0) for individuals with a high GRS compared with those with a low GRS across nine time points after controlling for sex, ancestry, renal status, dialysis, disease duration, treatment, depression, smoking and education, as well as time-dependent confounding of missing visits. Individual single-nucleotide polymorphism (SNP) analyses revealed that 12 of the 41 variants were significantly associated with clinically relevant changes in SLAQ scores across time points eight and nine after controlling for multiple testing. Results based on sophisticated causal modeling of longitudinal data in a large patient cohort suggest that individual SLE risk variants may influence disease activity over time. Our findings also emphasize a role for other biological or environmental factors.

Indexed as

Genetic Predisposition to DiseaseCohort StudiesFemaleHumansLikelihood FunctionsLongitudinal StudiesLupus Erythematosus, SystemicMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsSurveys and Questionnaires

Identifiers

PMID27467283
PMCPMC5008986

What OpenQuestion holds

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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.