Evidence map›Paper›PMID 22837712›Full record

Trial reportInternational journal of molecular sciences2012

DNA polymorphisms of the lipoprotein lipase gene and their association with coronary artery disease in the Saudi population.

Abdulaziz A Al-Jafari, Mohamed S Daoud, Abdulelah F Mobeirek, Mohammad S Al Anazi

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Lipoprotein Lipase (LPL) Polymorphism and the Risk of Coronary Artery Disease: A Meta-Analysis.International journal of environmental research and public health · 2017
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Associations betweenBioscience reports · 2018
    Article
  10. Article
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 1 institution in 1 country.

Abdulaziz A Al-JafariDepartment of Biochemistry, Faculty of Science, King Saud University, 11451, Saudi Arabia.
Mohamed S DaoudDepartment of Biochemistry, Faculty of Science, King Saud University, 11451, Saudi Arabia.
Abdulelah F MobeirekCardiac Sciences Department, Faculty of Medicine, King Saud University, 11472, Saudi Arabia.
Mohammad S Al AnaziDepartment of Biochemistry, Faculty of Science, King Saud University, 11451, Saudi Arabia.
King Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledCoronary heart disease (CHD) is a major health problem and a major cause of death in most countries. Evidence has been presented that gene polymorphisms (HindIII, PvuII and Ser447Ter) of lipoprotein lipase (LPL) are risk factors of coronary artery disease (CAD).

aimOur objective of the present investigation was to determine whether 3 LPL polymorphisms (LPL-HindIII, LPL-PvuII and LPL-Ser447Ter) can be considered as independent risk factors for CAD in the Saudi population.

methodsWe recruited 120 CAD subjects, confirmed angiographically with identical ethnic backgrounds and 65 control subjects. Polymerase chain reaction-restriction fragment length polymorphisms (RFLP) technique was used to detect the polymorphisms of the LPL gene. RESULTS AND

conclusionFor the HindIII genotype, within the CAD group, the frequencies of the H(+)H(+) were found in 50.8%, whereas 44.2% carried the H(-)H(+) genotype, and 5% carried the H(-)H(-) genotype. Within the control group, the H(+)H(+) genotype was found in 44.6%, whereas 35.4% carried the H(-)H(+) genotype, 20% carried the H(-)H(-) genotype. The odds ratio (OR) of HindIII genotype H(+)H(+)vs. H(-)H(-) genotype at 95% Confidence Interval (CI) were 4.6 (1.57-13.2) and p < 0.005, hence showing no significant association with CAD. For the PvuII genotype, within the CAD group the frequencies of the P(+)P(+) found in 41.7% whereas 43.3.2% carried the P(-)P(+) genotype, and 15% carried the P(-)P(-) genotype. Within the control group the P(+)P(+) was found in 38.5%, 43.0% carried the P(-)P(+) genotype, and 18.5% carried the P(-)P(-) genotype. The OR of PvuII genotype P(+)P(+)vs. P(-)P(-) genotypes (95% CI) is 1.33 and p = 0.52; hence, it was also insignificant to show association with the disease. For the Ser447Ter genotype, within the CAD group, the frequencies of the C/C found in 83.3%, whereas 16.7% carried the C/G genotype. Within the control group, the C/C was found in 87.7% and 12.3% carried the C/G genotype. We did not get any GG genotypes in control as well as patients for this gene. It can be concluded that C allele of gene masks the presence of G allele in the Saudi population. The OR of CG + GG vs. CC (95% CI) is 1.43 from 0.59 to 3.44 which is insignificant. Hence this gene also has no significant association with CAD in the Saudi population.

Indexed as

AllelesGenotypePolymorphism, GeneticAdultAgedCoronary DiseaseFemaleHumansLipoprotein LipaseMaleMiddle AgedSaudi ArabiaLipoprotein LipaseLPL protein, humancoronary artery diseasegenotypeslipoprotein lipaserestrictions fragmentSaudi populations and polymorphism

Identifiers

PMID22837712
PMCPMC3397544
OpenAlexW2038776814

What OpenQuestion holds

Textmetadata
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.