Evidence map›Paper›PMID 34386016›Full record

ArticleFrontiers in immunology2021

Genetically Determined Chronic Low-Grade Inflammation and Hundreds of Health Outcomes in the UK Biobank and the FinnGen Population: A Phenome-Wide Mendelian Randomization Study.

Shucheng Si, Jiqing Li, Marlvin Anemey Tewara, Fuzhong Xue

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 3 pooled it
9.7field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Circulating Copper and Liver Cancer.Biological trace element research · 2023
    Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Shucheng SiDepartment of Biostatistics, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jiqing LiDepartment of Biostatistics, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
Marlvin Anemey TewaraCenter for Health Promotion and Research (Former Tuberculosis Reference Laboratory), Bamenda, Cameroon.
Fuzhong XueDepartment of Biostatistics, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shandong University · CNUniversity of Bamenda · CM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: C-reactive protein (CRP) has been used as a biomarker of chronic low-grade inflammation in observational studies. We aimed to determine whether genetically determined CRP was associated with hundreds of human phenotypes to guide anti-inflammatory interventions. Methods: We used individual data from the UK Biobank to perform a phenome-wide two-stage least squares (2SLS) Mendelian randomization (MR) analysis for CRP with 879 diseases. Summary-level data from the FinnGen consortium were utilized to perform phenome-wide two-sample MR analysis on 821 phenotypes. Systematic two-sample MR methods included MR-IVW, MR-WME, MR-Mod, and MR-PRESSO as sensitivity analyses combined with multivariable MR to identify robust associations. Genetic correlation analysis was applied to identify shared genetic risks. Results: We found genetically determined CRP was robustly associated with 15 diseases in the UK Biobank and 11 diseases in the FinnGen population ( Conclusions: Genetically determined CRP was robustly associated with several diseases in the UK Biobank and the FinnGen population, but could not be replicated, suggesting heterogeneous and non-repeatable effects of CRP across populations. This implies that interventions at CRP are unlikely to result in decreased risk for most human diseases in the general population but may benefit specific high-risk populations. The limited causal evidence and potential double-sided effects remind us to be cautious about CRP interventions.

Indexed as

Genetic Predisposition to DiseasePhenotypeBiomarkersChronic DiseaseC-Reactive ProteinFemaleGenetic Association StudiesHumansInflammationMaleMendelian Randomization AnalysisPatient Outcome AssessmentPopulation SurveillanceProteomeProteomicsUnited KingdomBiomarkersC-Reactive ProteinProteomecausalityC-reactive proteininflammationMendelian randomizationphenome-wide association study (PheWAS)

Identifiers

PMID34386016
PMCPMC8353321
OpenAlexW3187057073

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.