Evidence map›Paper›PMID 29775600›Full record

SynthesisGastroenterology2018

Variation in Interleukin 6 Receptor Gene Associates With Risk of Crohn's Disease and Ulcerative Colitis.

Constantinos A Parisinos, Stylianos Serghiou, Michail Katsoulis, Marc Jonathan George, Riyaz S Patel, Harry Hemingway, Aroon D Hingorani

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Article
  5. Molecules (Basel, Switzerland) · 2025
    Article
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  8. Review
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  16. Nutrients · 2022
    Article
  17. Human Genomics and Drug Development.Cold Spring Harbor perspectives in medicine · 2022
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Constantinos A ParisinosInstitute of Health Informatics Research, Faculty of Population Health Sciences, University College London, London, UK. Electronic address: c.parisinos@ucl.ac.uk.
Stylianos SerghiouHealth Research and Policy, Epidemiology, Stanford University, Stanford, CA.
Michail KatsoulisInstitute of Health Informatics Research, Faculty of Population Health Sciences, University College London, London, UK.
Marc Jonathan GeorgeCentre for Clinical Pharmacology, Division of Medicine, University College London, London, UK.
Riyaz S PatelInstitute of Cardiovascular Science, Faculty of Population Health Sciences, University College London, London, UK.
Harry HemingwayInstitute of Health Informatics Research, Faculty of Population Health Sciences, University College London, London, UK.
Aroon D HingoraniInstitute of Cardiovascular Science, Faculty of Population Health Sciences, University College London, London, UK.
University College London · GBStanford University · US

Funding

British Heart Foundation FS/14/76/30933British Heart Foundation FS/18/5/33319Medical Research Council MR/K006584/1Wellcome TrustWellcome Trust 206274/Z/17/Z
6 · The paper itself

Abstract

Interleukin 6 (IL6) is an inflammatory cytokine; signaling via its receptor (IL6R) is believed to contribute to development of inflammatory bowel diseases (IBD). The single nucleotide polymorphism rs2228145 in IL6R associates with increased levels of soluble IL6R (s-IL6R), as well as reduced IL6R signaling and risk of inflammatory disorders; its effects are similar to those of a therapeutic monoclonal antibody that blocks IL6R signaling. We used the effect of rs2228145 on s-IL6R level as an indirect marker to investigate whether reduced IL6R signaling associates with risk of ulcerative colitis (UC) or Crohn's disease (CD). In a genome-wide meta-analysis of 20,550 patients with CD, 17,647 patients with UC, and more than 40,000 individuals without IBD (controls), we found that rs2228145 (scaled to a 2-fold increase in s-IL6R) was associated with reduced risk of CD (odds ratio 0.876; 95% confidence interval 0.822-0.933; P = .00003) or UC (odds ratio 0.932; 95% confidence interval 0.875-0.996; P = .036). These findings indicate that therapeutics designed to block IL6R signaling might be effective in treatment of IBD.

Indexed as

Genetic Predisposition to DiseaseColitis, UlcerativeCrohn DiseaseGenotypeHumansPolymorphism, Single NucleotideReceptors, Interleukin-6IL6R protein, humanReceptors, Interleukin-6Drug Target ValidationGeneticsMendelian RandomizationSNP

Identifiers

PMID29775600
PMCPMC6083435
OpenAlexW2804327066

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.