Evidence map›Paper›PMID 25902778›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015

Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk.

Mahmoud Merhi, Sally Demirdjian, Essa Hariri, Nada Sabbah, Sonia Youhanna, Michella Ghassibe-Sabbagh, Joseph Naoum, Marc Haber, Raed Othman, Samer Kibbani and 8 more

Abstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. An updated analysis on the association ofThe Journal of international medical research · 2022
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  15. A tagging ALOX5AP polymorphism and risk of ischemic stroke in a northeastern Chinese Han population.International journal of clinical and experimental medicine · 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

18 authors at 5 institutions in 2 countries.

Mahmoud MerhiSchool of Medicine, Lebanese American University, P.O Box 36, Byblos, Lebanon.
Sally Demirdjian
Essa Hariri
Nada Sabbah
Sonia Youhanna
Michella Ghassibe-Sabbagh
Joseph Naoum
Marc Haber
Raed Othman
Samer Kibbani
Elie Chammas
Roy Kanbar
Hamid El Bayeh
Youssef Chami
Antoine Abchee
Daniel E Platt
Pierre Zalloua
Georges Khazen
Lebanese American University · LBRafik Hariri University Hospital · LBAmerican University of Beirut · LBBrandeis University · USIBM (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of inflammation in coronary artery disease (CAD) pathogenesis is well recognized. Moreover, smoking inhalation increases the activity of inflammatory mediators through an increase in leukotriene synthesis essential in atherosclerosis pathogenesis.

aimThe aim of this study is to investigate the effect of "selected" genetic variants within the leukotriene (LT) pathway and other variants on the development of CAD.

methodsCAD was detected by cardiac catheterization. Logistic regression was performed to investigate the association of smoking and selected susceptibility variants in the LT pathway including ALOX5AP, LTA4H, LTC4S, PON1, and LTA as well as CYP1A1 on CAD risk while controlling for age, gender, BMI, family history, diabetes, hyperlipidemia, and hypertension.

resultsrs4769874 (ALOX5AP), rs854560 (PON1), and rs4646903 (CYP1A1 MspI polymorphism) are significantly associated with an increased risk of CAD with respective odds ratios of 1.53703, 1.67710, and 1.35520; the genetic variant rs9579646 (ALOX5AP) is significantly associated with a decreased risk of CAD (OR 0.76163). Moreover, a significant smoking-gene interaction is determined with CYP1A1 MspI polymorphism rs4646903 and is associated with a decreased risk of CAD in current smokers (OR 0.52137).

conclusionThis study provides further evidence that genetic variation of the LT pathway, PON1, and CYP1A1 can modulate the atherogenic processes and eventually increase the risk of CAD in our study population. Moreover, it also shows the effect of smoking-gene interaction on CAD risk, where the CYP1A1 MspI polymorphism revealed a decreased risk in current smokers.

Indexed as

AgedAllelesAryldialkylphosphataseCoronary Artery DiseaseCross-Sectional StudiesCytochrome P-450 CYP1A1FemaleGenetic VariationHumansInflammationLeukotrienesMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsSmokingAryldialkylphosphataseCytochrome P-450 CYP1A1LeukotrienesPON1 protein, human

Identifiers

PMID25902778
OpenAlexW1967243574

What OpenQuestion holds

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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.