Evidence map›Paper›PMID 8370576›Full record

ArticleHuman genetics1993

Relation of cardiovascular risk factors to atherosclerosis in type III hyperlipoproteinemia.

G Feussner, A Wagner, R Ziegler

Abstract read
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In one paragraph

Article in Human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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

3 authors.

G FeussnerAbteilung Innere Medizin I, Schwerpunkt Endokrinologie und Stoffwechsel, Medizinische Universiätsklinik Heidelberg, Germany.
A Wagner
R Ziegler

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The familial lipoprotein disorder type III hyperlipoproteinemia (HPL) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation among affected individuals in susceptibility to cardiovascular disease (CVD). We studied the influence of independent risk factors for atherosclerosis in 67 patients with clinically overt type III HPL and homozygosity for apolipoprotein (apo) E2. Among the different risk factors (lipid and lipoprotein levels, age, sex, body mass index, smoking status, hypertension, and diabetes mellitus) there was only a statistically significant difference in age between 25 patients with atherosclerosis and 42 patients without atherosclerosis. Serum lipoprotein (a), [Lp, (a)], levels were 30.6% higher in the atherosclerosis group, but this was not statistically significant. We conclude that (in contrast to familial hypercholesterolemia) elevated Lp (a) concentrations may not be regarded as a component of the clinical syndrome of type III HPL.

Indexed as

Age FactorsApolipoprotein E2Apolipoproteins EArteriosclerosisChi-Square DistributionDisease SusceptibilityFemaleHomozygoteHumansHyperlipoproteinemia Type IIIHypertensionLipoprotein(a)MaleMiddle AgedRisk FactorsSex FactorsApolipoprotein E2Apolipoproteins ELipoprotein(a)

Identifiers

PMID8370576

What OpenQuestion holds

Textmetadata
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.