Evidence mapPaperPMID 2394828Full record

ArticleThe Journal of clinical investigation1990

Phenotypic expression of heterozygous lipoprotein lipase deficiency in the extended pedigree of a proband homozygous for a missense mutation.

D E Wilson, M Emi, P H Iverius, A Hata, L L Wu, E Hillas, R R Williams, J M Lalouel

Registry-linked trialAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00005139 (Characterization Of Coronary Prone Pedigrees), which is not on this map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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.

NCT00005139 completednot on this map

Characterization Of Coronary Prone Pedigrees

TypeobservationalSponsorUniversity of UtahRan1977 to 1991ConditionsCardiovascular Diseases, Coronary Disease, Heart Diseases
3 · Its place in the literature

Who cites it

25 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Low circulating PCSK9 levels inFrontiers in genetics · 2022
    Article
  7. An upstream enhancer regulatesJournal of lipid research · 2019
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors.

D E WilsonDepartment of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City 84132.
M Emi
P H Iverius
A Hata
L L Wu
E Hillas
R R Williams
J M Lalouel

Funding

CHARACTERIZATION OF CORONARY PRONE PEDIGREESR01HL021088 · UNIVERSITY OF UTAH · 1985 to 1990
EFFECTS OF SEX STEROIDS OF ADIPOCYTE LIPOPROTEIN LIPASER29HL039595 · UNIVERSITY OF UTAH · 1988 to 1992
NCRR NIH HHS RR-00064NHLBI NIH HHS HL-21088NHLBI NIH HHS HL-39595
6 · The paper itself

Abstract

Familial lipoprotein lipase (LPL) deficiency is a rare genetic disorder accompanied by well-characterized manifestations. The phenotypic expression of heterozygous LPL deficiency has not been so clearly defined. We studied the pedigree of a proband known to be homozygous for a mutation resulting in nonfunctional LPL. Hybridization of DNA from 126 members with allele-specific probes detected 29 carriers of the mutant allele. Adipose tissue LPL activity, measured previously, was reduced by 50% in carriers, but did not reliably distinguish them from noncarriers. Carriers were prone to the expression of a form of familial hypertriglyceridemia characterized by increased plasma triglyceride, VLDL cholesterol and apolipoprotein B, and decreased LDL and HDL cholesterol concentrations. These manifestations were age modulated, with conspicuous differences between carriers and noncarriers observed only after age 40. Several noncarriers exhibited similar lipid abnormalities, but without the inverse relationship between VLDL cholesterol and LDL cholesterol noted among carriers. In addition to age and carrier status, the potentially reversible conditions, obesity, hyperinsulinemia and lipid-raising drug use were contributory. Thus heterozygous lipoprotein lipase deficiency, together with age-related influences, may account for a form of familial hypertriglyceridemia.

Indexed as

Adipose TissueAdultAgedAge FactorsBase SequenceChildCholesterol, HDLCholesterol, LDLCholesterol, VLDLDiabetes ComplicationsDiscriminant AnalysisFemaleHeterozygoteHumansLipoprotein LipaseMaleCholesterol, HDLCholesterol, LDLCholesterol, VLDLLipoprotein LipaseOligonucleotidesTriglycerides

Identifiers

PMID2394828
PMCPMC296788

What Socratic holds

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Read underepoch 390

Registered trials

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 Socratic graph.