Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-12-3
pubmed:abstractText
In order to characterize the lipoprotein abnormalities in familial combined hyperlipidemia (FCHL) and to describe factors associated with the stability of the FCHL phenotype during 20-year follow-up, 287 individuals from 48 families with FCHL originally identified in the early 1970s (baseline) were studied. Hyperlipidemia was defined as lipid-lowering medication use, or > or =age- and sex-specific 90th percentile for triglycerides or cholesterol. Triglyceride, cholesterol and medical history data were obtained at baseline and 20-year follow-up. Additional follow-up measures included HDL-C, LDL-C, LDL particle size, lipoprotein(a), apolipoprotein (apo) A-I, apoB, and apoE polymorphism. Longitudinally, two-thirds of relatives were consistently normolipidemic or hyperlipidemic, and one third were discordant for hyperlipidemic status at baseline and 20-year follow-up. Individuals with hyperlipidemia at baseline and/or follow-up had higher apoB levels than those with consistently normal lipids (P<0.05), whereas small LDL size was associated with concurrent hyperlipidemia. Among individuals who were normolipidemic at baseline, the following variables were independently associated with development of hyperlipidemia over 20 years: older age at baseline, male sex, greater increase in BMI during follow-up, and apoE alleles epsilon 2 or epsilon 4. In conclusion, apoB is associated with hyperlipidemia and apoE polymorphism is associated with later onset of hyperlipidemia in FCHL.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9150
pubmed:author
pubmed:issnType
Print
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
471-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11730829-Adult, pubmed-meshheading:11730829-Age Distribution, pubmed-meshheading:11730829-Apolipoprotein A-I, pubmed-meshheading:11730829-Apolipoproteins, pubmed-meshheading:11730829-Child, pubmed-meshheading:11730829-Cholesterol, HDL, pubmed-meshheading:11730829-Cholesterol, LDL, pubmed-meshheading:11730829-Female, pubmed-meshheading:11730829-Follow-Up Studies, pubmed-meshheading:11730829-Humans, pubmed-meshheading:11730829-Hyperlipidemia, Familial Combined, pubmed-meshheading:11730829-Incidence, pubmed-meshheading:11730829-Lipoproteins, pubmed-meshheading:11730829-Longitudinal Studies, pubmed-meshheading:11730829-Male, pubmed-meshheading:11730829-Middle Aged, pubmed-meshheading:11730829-Pedigree, pubmed-meshheading:11730829-Polymorphism, Genetic, pubmed-meshheading:11730829-Probability, pubmed-meshheading:11730829-Prospective Studies, pubmed-meshheading:11730829-Reference Values, pubmed-meshheading:11730829-Risk Factors, pubmed-meshheading:11730829-Sex Distribution
pubmed:year
2001
pubmed:articleTitle
Lipoprotein and apolipoprotein abnormalities in familial combined hyperlipidemia: a 20-year prospective study.
pubmed:affiliation
Department of Medicine, School of Medicine, University of Washington, Box 356429, Seattle, WA 98195, USA. mcneely@u.washington.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.