Evidence map›Paper›PMID 24651583›Full record

ArticleInflammatory bowel diseases2014

Genetic polymorphisms in metabolizing enzymes modifying the association between smoking and inflammatory bowel diseases.

Ashwin N Ananthakrishnan, Deanna D Nguyen, Jenny Sauk, Vijay Yajnik, Ramnik J Xavier

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 4 pooled it
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 4 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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  10. Environmental risk factors for inflammatory bowel disease.United European gastroenterology journal · 2022
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  18. Epidemiology and risk factors for IBD.Nature reviews. Gastroenterology & hepatology · 2015
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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

5 authors at 2 institutions in 1 country.

Ashwin N Ananthakrishnan*Division of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts; †Harvard Medical School, Boston, Massachusetts; ‡Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts; and §Broad Institute, Cambridge, Massachusetts.
Deanna D Nguyen
Jenny Sauk
Vijay Yajnik
Ramnik J Xavier
Harvard University · USBroad Institute · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Ramnik J Xavier · 1991 to 2026
$35.3M
Universite de Montreal IBD Genetics Research CenterU01DK062432 · NIDDK · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI John D. Rioux · 2002 to 2026
$9.6M
Identification of the IBD genes on chromosomes 3p and 6pR01DK064869 · NIDDK · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI RIOUX, JOHN D. · 2003 to 2016
$7.8M
Genetic predictors of anti-TNF treatment response and infections in IBDK23DK097142 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ANANTHAKRISHNAN, ASHWIN N · 2012 to 2016
$846k
NIDDK NIH HHS K23 DK097142NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK064869NIDDK NIH HHS U01 DK062432
6 · The paper itself

Abstract

backgroundCigarette smoking is a well-established environmental risk factor for Crohn's disease (CD) and ulcerative colitis (UC). The exact mechanism of its effect remains unexplained. Genetic polymorphisms in metabolizing enzymes may influence susceptibility to the effect of smoking and shed light on its mechanism of action.

methodsWe used a prospective cohort of patients with CD, UC, and healthy controls. Smoking status was defined as current, former, or never smoking. Patients were genotyped for polymorphisms in CYP2A6, glutathione transferase enzymes (GSTP1 and GSTM1), NAD(P)H quinone oxidoreductase (NQO), and heme oxygenase 1 using a Sequenom platform. Multivariate logistic regression models with CD or UC as the outcome, stratified by genotype, were developed and interaction P-values calculated.

resultsOur study included 634 patients with CD, 401 with UC, and 337 healthy controls. Ever smokers had an increased risk of CD (odds ratio = 3.88, 95% confidence interval = 2.35-6.39) compared with nonsmokers among patients with AG/AA genotypes at CYP2A6. However, ever smoking was not associated with CD among patients with the AA genotype (Pinteraction = 0.001). Former smoking was associated with an increased risk for UC only in the presence of GG/AG genotypes for GSTP1 but not in those with the AA genotype (Pinteraction = 0.012). Polymorphisms at the NQO and HMOX loci did not demonstrate a statistically significant interaction with smoking and risk of CD or UC.

conclusionsGenetic polymorphisms in metabolizing enzymes may influence the association between smoking and CD and UC. Further studies of gene-environment interaction in inflammatory bowel disease are warranted.

Indexed as

AdolescentAdultBiomarkersCase-Control StudiesColitis, UlcerativeCrohn DiseaseCytochrome P-450 CYP2A6FemaleFollow-Up StudiesGenetic Predisposition to DiseaseGlutathione S-Transferase piGlutathione TransferaseHeme Oxygenase-1HumansMaleMiddle AgedBiomarkersCYP2A6 protein, humanCytochrome P-450 CYP2A6Glutathione S-Transferase piGlutathione TransferaseGSTP1 protein, humanHeme Oxygenase-1NAD(P)H Dehydrogenase (Quinone)NQO1 protein, human

Identifiers

PMID24651583
PMCPMC4113010
OpenAlexW2090089483

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.