Evidence map›Paper›PMID 33214142›Full record

SynthesisNeurology(R) neuroimmunology & neuroinflammation2021

Mendelian randomization study shows no causal effects of serum urate levels on the risk of MS.

Adil Harroud, J Brent Richards, Sergio E Baranzini

Abstract readMeta-Analysis
In one paragraph

Synthesis in Neurology(R) neuroimmunology & neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Current and Future Biomarkers in Multiple Sclerosis.International journal of molecular sciences · 2022
    Review
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

3 authors.

Adil HarroudFrom the Department of Neurology (A.H., S.E.B.), University of California San Francisco, California; Weill Institute for Neurosciences (A.H., S.E.B.), University of California San Francisco, California; Centre for Clinical Epidemiology (J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Department of Human Genetics (J.B.R.), McGill University, Montreal, Quebec, Canada; Department of Medicine (J.B.R.), McGill University Montreal, Quebec, Canada; Department of Epidemiology (J.B.R.), Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada; Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, United Kingdom; Institute for Human Genetics (S.E.B.), University of California San Francisco, California; and Bakar Computational Health Sciences Institute (S.E.B.), University of California San Francisco, California.ORCID 0000-0003-2616-7274
J Brent RichardsFrom the Department of Neurology (A.H., S.E.B.), University of California San Francisco, California; Weill Institute for Neurosciences (A.H., S.E.B.), University of California San Francisco, California; Centre for Clinical Epidemiology (J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Department of Human Genetics (J.B.R.), McGill University, Montreal, Quebec, Canada; Department of Medicine (J.B.R.), McGill University Montreal, Quebec, Canada; Department of Epidemiology (J.B.R.), Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada; Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, United Kingdom; Institute for Human Genetics (S.E.B.), University of California San Francisco, California; and Bakar Computational Health Sciences Institute (S.E.B.), University of California San Francisco, California.
Sergio E BaranziniFrom the Department of Neurology (A.H., S.E.B.), University of California San Francisco, California; Weill Institute for Neurosciences (A.H., S.E.B.), University of California San Francisco, California; Centre for Clinical Epidemiology (J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Department of Human Genetics (J.B.R.), McGill University, Montreal, Quebec, Canada; Department of Medicine (J.B.R.), McGill University Montreal, Quebec, Canada; Department of Epidemiology (J.B.R.), Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada; Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, United Kingdom; Institute for Human Genetics (S.E.B.), University of California San Francisco, California; and Bakar Computational Health Sciences Institute (S.E.B.), University of California San Francisco, California. sergio.baranzini@ucsf.edu.ORCID 0000-0003-0067-194X

Funding

CIHRDepartment of HealthMedical Research CouncilWellcome Trust
6 · The paper itself

Abstract

objectiveTo examine whether lifelong genetically increased serum urate levels, a potent antioxidant, contribute to MS susceptibility using Mendelian randomization (MR).

methodsThis 2-sample MR study included 25 independent genetic variants strongly associated with serum urate levels in a genome-wide association study meta-analysis of 140,949 individuals. Effects on the risk of MS were assessed with summary statistics from 3 large-scale MS genetic data sets totaling 61,667 MS cases and 86,806 controls from the International MS Genetic Consortium. Multiple sensitivity analyses were performed to evaluate the assumptions of MR and remove potentially pleiotropic variants.

resultsUsing inverse-variance weighted MR, we found no evidence for a causal effect of serum urate level on the risk of MS in any of the cohorts (MS1: OR 0.99 per each mg/dL unit increase in urate, 95% CI 0.89-1.08,

conclusionThis MR study does not support a clinically relevant causal effect of serum urate levels on the risk of MS.

Indexed as

Genome-Wide Association StudyHumansMendelian Randomization AnalysisMultiple SclerosisUric AcidUric Acid

Identifiers

PMID33214142
PMCPMC7694579

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.