Evidence map›Paper›PMID 22855291›Full record

ArticleDigestive diseases and sciences2012

The role of 5-HTT LPR and GNβ3 825C>T polymorphisms and gene-environment interactions in irritable bowel syndrome (IBS).

Yuri A Saito, Joseph J Larson, Elizabeth J Atkinson, Euijung Ryu, Ann E Almazar, Gloria M Petersen, Nicholas J Talley

Open access · greenAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. G protein beta 3(Oncotarget · 2018
    Article
  7. Genetic epidemiology of irritable bowel syndrome.World journal of gastroenterology · 2015
    Review
  8. Review
  9. Article
  10. Review
  11. Molecular basis of the irritable bowel syndrome.World journal of gastroenterology · 2014
    Review
  12. Article
  13. The role of genetics in IBS.Gastroenterology clinics of North America · 2011
    Review
  14. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Yuri A SaitoDivision of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. saito.yuri@mayo.edu
Joseph J Larson
Elizabeth J Atkinson
Euijung Ryu
Ann E Almazar
Gloria M Petersen
Nicholas J Talley
Mayo Clinic · USUniversity of Newcastle Australia · AU

Funding

Genetic epidemiology of irritable bowel syndrome (IBS)K23DK066271 · NIDDK · MAYO CLINIC ROCHESTER · PI SAITO LOFTUS, YURI ANN · 2004 to 2008
$630k
NIDDK NIH HHS K23 DK066271NIDDK NIH HHS K23 DK66271
6 · The paper itself

Abstract

backgroundSmaller studies have evaluated SLC6A4 5-HTTLPR and GNβ3 825C>T polymorphisms in IBS, and interactions between 5-HTT LPR with life events have been reported in the psychiatric literature, but gene-environment studies in IBS are lacking.

aimsThe purpose of this study was to assess the association of two polymorphisms with IBS and age of onset, and whether there are gene-environment interactions with IBS.

methodsOutpatients with IBS and controls completed a validated questionnaire and provided blood for DNA. Comparisons of genotype/allele frequencies between cases and controls were performed with logistic regression. Linear regression was used to evaluate the association between the variants and age of onset. Environmental variables tested included abuse, parental alcohol abuse, parental psychiatric disorders, and gastrointestinal infections.

resultsGenotyping was performed in 385 cases and 262 controls with median age of 50 years (range, 18.0-70.0) and 498 (77 %) females. The IBS subtype distribution among cases was: 102 (26 %) D-IBS, 40 (10 %) C-IBS, 125 (32 %) M-IBS, 118 (31 %) other. No association was observed between IBS or age of onset and both variants. Significant interactions were observed between GI infection and the GNβ3 825T allele. For those reporting gastrointestinal infection, the OR for IBS was 3.9 (95 % CI 1.2-12.7) whereas the OR was 0.86 (95 % CI 0.65-1.13) for those without prior infection.

conclusionsThere was a significant interaction between the GNβ3 polymorphism and infection in the development of IBS, suggesting that its etiology is the result of a combination of specific genetic and environmental risk factors.

Indexed as

Gene-Environment InteractionGenetic Predisposition to DiseasePolymorphism, GeneticAdolescentAdultAgedAge of OnsetCase-Control StudiesEpigenesis, GeneticFemaleHeterotrimeric GTP-Binding ProteinsHumansIrritable Bowel SyndromeMaleMiddle AgedOdds RatioG-protein beta3 subunitHeterotrimeric GTP-Binding ProteinsSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, human

Identifiers

PMID22855291
PMCPMC3912694
OpenAlexW2027076070

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Registered trials

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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.