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Short Communication

Genetic Determination of Acute Phase Reactant Levels: The Strong Heart Study

Best L.G.a · North K.E.b · Tracy R.P.c · Lee E.T.d · Howard B.V.e · Palmieri V.f · MacCluer J.W.g

Author affiliations

aMissouri Breaks Industries Research Inc, Timber Lake, S.Dak., bUniversity of North Carolina, Chapel Hill,N.C., cLaboratory for Clinical Biochemistry Research, University of Vermont, Burlington, Vt., dUniversity of Oklahoma Health Sciences Center, Oklahoma City, Okla., eMedstar Research Institute, Washington, D.C., fWeill Medical College of Cornell University, New York, N.Y., and gSouthwest Foundation for Biomedical Research, SanAntonio,Tex., USA

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Hum Hered 2004;58:112–116

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Article / Publication Details

First-Page Preview
Abstract of Short Communication

Received: March 16, 2004
Accepted: August 20, 2004
Published online: February 10, 2005
Issue release date: February 2005

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 3

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: https://www.karger.com/HHE

Abstract

Objective: C-reactive protein (CRP), fibrinogen and plasminogen activating inhibitor-1 (PAI-1) are acute phase reactants (APRs); and high levels are indicative of physiologic inflammatory responses. Basal (non-stimulated) APR levels have also been shown to predict atherosclerotic complications in a number of populations. We sought to determine the relative contributions of genetic and environmental factors influencing basal serum levels of APRs. Methods: This study used univariate quantitative genetic analyses to partition the phenotypic variance of these APRs into their additive genetic and environmental components using maximum likelihood variance decomposition methods. Bivariate analyses were done to detect genetic correlation between APRs. The computer program SOLAR was used to perform these analyses. Results: The Strong Heart Study (SHS) includes information on approximately 1,294 American Indian relative pairs. The proportion of variance due to environmental and acquired covariates affecting these APRs was modest, ranging from 16–20%. The proportion of variance due to genetic factors (heritability) ranged from 24–46%. In addition, there were significant genetic correlations between CRP/fibrinogen (ρ = 0.41 ± 0.12) and CRP/PAI-1 (ρ = 0.46 ± 0.19); but not between fibrinogen/PAI-1. Conclusion: In the SHS cohort, the levels of APRs are determined to a substantial degree by genetic influences, and CRP shares common genetic determinants with fibrinogen and PAI-1.

© 2004 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Short Communication

Received: March 16, 2004
Accepted: August 20, 2004
Published online: February 10, 2005
Issue release date: February 2005

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 3

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: https://www.karger.com/HHE


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