Evidence map›Paper›PMID 19710913›Full record

ArticlePloS one2009

Both paraoxonase-1 genotype and activity do not predict the risk of future coronary artery disease; the EPIC-Norfolk Prospective Population Study.

Rakesh S Birjmohun, Menno Vergeer, Erik S G Stroes, Manjinder S Sandhu, Sally L Ricketts, Michael W Tanck, Nicholas J Wareham, J Wouter Jukema, John J P Kastelein, Kay-Tee Khaw and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
4.7field-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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Homocysteine Thiolactone Detoxifying Enzymes and Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  7. Paraoxonase 1 and atherosclerosis.Frontiers in cardiovascular medicine · 2023
    Review
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  10. Article
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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

11 authors at 5 institutions in 2 countries.

Rakesh S BirjmohunDepartment of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. r.s.birjmohun@amc.uva.nl
Menno Vergeer
Erik S G Stroes
Manjinder S Sandhu
Sally L Ricketts
Michael W Tanck
Nicholas J Wareham
J Wouter Jukema
John J P Kastelein
Kay-Tee Khaw
S Matthijs Boekholdt
Academic Medical Center · NLUniversity of Cambridge · GBLeiden University Medical Center · NLMedical Research Council · GBUniversity of Amsterdam · NL

Funding

British Heart Foundation PG/08/094/26019Cancer Research UKDepartment of HealthMedical Research Council G0401527Medical Research Council G0801566Wellcome Trust
6 · The paper itself

Abstract

backgroundParaoxonase-1 (PON1) is an antioxidant enzyme, that resides on high-density lipoprotein (HDL). PON1-activity, is heavily influenced by the PON1-Q192R polymorphism. PON1 is considered to protect against atherosclerosis, but it is unclear whether this relation is independent of its carrier, HDL. In order to evaluate the atheroprotective potential of PON1, we assessed the relationships among PON1-genotype, PON1-activity and risk of future coronary artery disease (CAD), in a large prospective case-control study. METHODOLOGY/PRINCIPAL

findingsCases (n = 1138) were apparently healthy men and women aged 45-79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n = 2237) were matched by age, sex and enrollment time. PON1-activity was similar in cases and controls (60.7+/-45.3 versus 62.6+/-45.8 U/L, p = 0.3) and correlated with HDL-cholesterol levels (r = 0.16, p<0.0001). The PON1-Q192R polymorphism had a profound impact on PON1-activity, but did not predict CAD risk (Odds Ratio [OR] per R allele 0.98[0.84-1.15], p = 0.8). Using conditional logistic regression, quartiles of PON1-activity showed a modest inverse relation with CAD risk (OR for the highest versus the lowest quartile 0.77[0.63-0.95], p = 0.01; p-trend = 0.06). PON1-activity adjusted for Q192R polymorphism correlated better with HDL-cholesterol (r = 0.26, p<0.0001) and more linearly predicted CAD risk (0.79[0.64-0.98], p = 0.03; p-trend = 0.008). However, these relationships were abolished after adjustment for HDL (particles-cholesterol-size) and apolipoproteinA-I (0.94[0.74-1.18], p-trend = 0.3). CONCLUSIONS/SIGNIFICANCE: This study, shows that PON1-activity inversely relates to CAD risk, but not independent of HDL, due to its close association with the HDL-particle. These data strongly suggest that a low PON1-activity is not a causal factor in atherogenesis.

Indexed as

AgedAryldialkylphosphataseAustriaCase-Control StudiesCoronary Artery DiseaseFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedPolymorphism, GeneticRisk FactorsAryldialkylphosphatasePON1 protein, human

Identifiers

PMID19710913
PMCPMC2728540
OpenAlexW2074053934

What OpenQuestion holds

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LicenceCC BY
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.