Evidence map›Paper›PMID 32430061›Full record

ArticleLipids in health and disease2020

Association of common gene-smoking interactions with elevated plasma apolipoprotein B concentration.

Nathalie Roy, Daniel Gaudet, Gérald Tremblay, Diane Brisson

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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 3 institutions in 1 country.

Nathalie RoyDepartment of Medicine, Université de Montréal, ECOGENE-21 Clinical and Translational Research Center, 930 Jacques-Cartier, Chicoutimi, Quebec, G7H 7K9, Canada.
Daniel GaudetDepartment of Medicine, Université de Montréal, ECOGENE-21 Clinical and Translational Research Center, 930 Jacques-Cartier, Chicoutimi, Quebec, G7H 7K9, Canada.
Gérald TremblayDepartment of Medicine, Université de Montréal, ECOGENE-21 Clinical and Translational Research Center, 930 Jacques-Cartier, Chicoutimi, Quebec, G7H 7K9, Canada.
Diane BrissonDepartment of Medicine, Université de Montréal, ECOGENE-21 Clinical and Translational Research Center, 930 Jacques-Cartier, Chicoutimi, Quebec, G7H 7K9, Canada. diane.brisson@ecogene21.org.ORCID http://orcid.org/0000-0002-9878-4346
Cégep de Chicoutimi · CAUniversité de Montréal · CAUniversité du Québec à Chicoutimi · CA

Funding

ECOGENE-21 N/A
6 · The paper itself

Abstract

backgroundIncreased apolipoprotein (apo) B level (hyperapoB) is a strong predictor of cardiovascular disease (CVD), even in patients who achieve recommended LDL-Cholesterol (LDL-C) goals. ApoB level, an important correlate of metabolic syndrome (MetS), is influenced by several gene-environment interactions. Some of them are rare and can explain a large proportion of apoB variance, whereas others more common have variable effects. The aim of this study was to evaluate the association of interaction between smoking and common hyperapoB gene variants (PPARα-L162V, lipoprotein lipase loss-of function mutation, apo e4 allele or apo E2/2 genotype) with plasma apoB concentrations, according to the expression of MetS.

methodsThis study was performed among 1798 subjects. Smoking was defined as non/mild smokers vs. moderate-to-heavy smokers. ApoB levels were determined using nephelometry. Logistic regression models were used to document interactions between smoking habits and the presence of hyperapoB gene variants on the relative odds to exhibit increased plasma apoB concentrations.

resultsAround 29% of individuals with a low-risk lipid profile without MetS component had hyperapoB. Smoking and the presence of hyperapoB gene variants tended to be associated with higher plasma apoB levels even in presence of low-LDL-C. There was a significant interaction (P = 0.04) between the presence of ≥1 gene variants and smoking on the risk to exhibit hyperapoB among subjects with low risk profile in primary prevention.

conclusionsCombination of life habits assessment and some common genes variants may detect a significant proportion of patients with increased apoB levels, and therefore a higher risk of CVD, who could have been initially perceived as low-risk.

Indexed as

Gene-Environment InteractionPolymorphism, GeneticApolipoprotein E4Apolipoproteins BFemaleHumansLipoprotein LipaseMaleMetabolic SyndromeMiddle AgedPPAR alphaQuebecSmokingApolipoprotein E4Apolipoproteins BLipoprotein LipasePPAR alphaPPARA protein, humanApolipoprotein BGene variantsSmoking

Identifiers

PMID32430061
PMCPMC7236958
OpenAlexW3027645220

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.