Evidence map›Paper›PMID 17660460›Full record

ArticleJournal of medical genetics2007

Estimating risks of common complex diseases across genetic and environmental factors: the example of Crohn disease.

C M Lewis, S C L Whitwell, A Forbes, J Sanderson, C G Mathew, T M Marteau

Open access · bronzeAbstract read
In one paragraph

Article in Journal of medical genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  11. An envirogenomic signature is associated with risk of IBD-related surgery in a population-based Crohn's disease cohort.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2013
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

C M LewisDepartment of Medical and Molecular Genetics, Division of Genetics and Molecular Medicine, King's College London School of Medicine, London, UK. cathryn.lewis@kcl.ac.uk
S C L Whitwell
A Forbes
J Sanderson
C G Mathew
T M Marteau
King's College London · GBGuy's and St Thomas' NHS Foundation Trust · GBGuy's Hospital · GBUniversity College London · GB

Funding

Medical Research Council G0500274Medical Research Council G0500274(73436)Wellcome Trust 068545/Z/02Wellcome Trust 072029Wellcome Trust 076024
6 · The paper itself

Abstract

backgroundProgress has been made in identifying mutations that confer susceptibility to complex diseases, with the prospect that these genetic risks might be used in determining individual disease risk.

aimTo use Crohn disease (CD) as a model of a common complex disorder, and to develop methods to estimate disease risks using both genetic and environmental risk factors.

methodsThe calculations used three independent risk factors: CARD15 genotype (conferring a gene dosage effect on risk), smoking (twofold increased risk for smokers), and residual familial risk (estimating the effect of unidentified genes, after accounting for the contribution of CARD15). Risks were estimated for high-risk people who are siblings, parents and offspring of a patient with CD.

resultsThe CD risk to the sibling of a patient with CD who smokes and carries two CARD15 mutations is approximately 35%, which represents a substantial increase on the population risk of 0.1%. In contrast, the risk to a non-smoking sibling of a patient with CD who carries no CARD15 mutations is 2%. Risks to parents and offspring were lower.

conclusionsHigh absolute risks of CD disease can be obtained by incorporating information on smoking, family history and CARD15 mutations. Behaviour modification through smoking cessation may reduce CD risk in these people.

Indexed as

Environmental ExposureAdolescentAdultBayes TheoremColitis, UlcerativeCrohn DiseaseEuropeFamily HealthFemaleGene DosageGenetic HeterogeneityGenetic Predisposition to DiseaseHumansMaleModels, GeneticNod2 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID17660460
PMCPMC2752174
OpenAlexW2114042086

What OpenQuestion holds

Textmetadata
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.