Evidence map›Paper›PMID 17727701›Full record

ArticleBMC medical genetics2007

The D9N, N291S and S447X variants in the lipoprotein lipase (LPL) gene are not associated with Type III hyperlipidemia.

David Evans, Frank U Beil

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-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

3 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Unraveling hyperlipidemia type III (dysbetalipoproteinemia), slowly.European journal of human genetics : EJHG · 2009
    Article
  3. 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

2 authors at 1 institution in 1 country.

David EvansEndokrinologie und Stoffwechsel, Medizinische Klinik III, Zentrum für Innere Medizin, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. evans@uke.uni-hamburg.de
Frank U Beil
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType III hyperlipidemia (Type III HLP) is associated with homozygosity for the epsilon2 allele of the APOE gene. However only about 10% of epsilon2 homozygotes develop Type III HLP and it is assumed that additional genetic and/or environmental factors are required for its development. Common variants in the LPL gene have been proposed as likely genetic co-factors.

methodsThe frequency of the LPL SNPs D9N, N291S and S447X in 100 patients with hyperlipidemia and APOE2/2 genotype has been determined and compared to that in healthy blood donors and patients with hyperlipidemia.

resultsThere were no statistically significant difference in the frequencies of the variants between APOE2/2 patients and controls.

conclusionIt is unlikely that the D9N, N291S or S447X variants in the LPL gene play an important role in the development of Type III HLP.

Indexed as

AdultAllelesApolipoprotein E2FemaleGenotypeHumansHyperlipoproteinemia Type IIILipoprotein LipaseMaleMiddle AgedPolymorphism, Single NucleotideApolipoprotein E2Lipoprotein Lipase

Identifiers

PMID17727701
PMCPMC2025595
OpenAlexW1988371852

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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.