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Concentrations of the atherogenic Lp(a) are elevated in familial hypercholesterolaemia: a sib pair and family analysis

Lingenhel, Arno, Kraft, Hans Georg, Kotze, Maritha, Peeters, Armand V, Kronenberg, Florian, Kruse, Rita, Utermann, Gerd·1998·European Journal of Human Genetics
DOI 10.1038/sj.ejhg.5200152
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Abstract

Lipoprotein(a) (Lp(a)) is a complex in human plasma assembled from low-density lipoprotein (LDL) and apolipoprotein(a) (apo(a)). High plasma concentrations of Lp(a) are a risk factor for coronary heart disease (CHD) in particular in patients with concomitant elevation of LDL. We have analysed for elevated Lp(a) levels in patients with familial hypercholesterolaemia (FH), a condition caused by mutations in the LDL receptor (LDLR) gene and characterised by high LDL, xanthomatosis and premature CHD. To avoid possible confusion by the apo(a) gene which is the major quantitative trait locus controlling Lp(a) in the population at large, we used a sib pair approach based on genotype information for both the LDLR and the apo(a) gene. We analysed 367 family members of 30 South African and 30 French Canadian index patients with FH for LDLR mutations and for apo(a) genotype. Three lines of evidence showed a significant effect of FH on Lp(a) levels: (1) Lp(a) values were significantly higher in FH individuals compared to non-FH relatives (p < 0.001), although the distribution of apo(a) alleles was not different in the two groups; (2) comparison of Lp(a) concentrations in 28 sib pairs, identical by descent (i.b.d.) at the apo(a) locus but non-identical for LDLR status, extracted from this large sample demonstrated significantly elevated Lp(a) concentrations in sibs with FH (p < 0.001); (3) single i.b.d. apo(a) alleles were associated with significantly higher Lp(a) concentrations (p < 0.0…

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  • Some studies of individuals with Familial Hypercholesterolemia have reported an increase in Lp(a) levels.

    “Some studies of individuals with Familial Hypercholesterolemia (FH) have reported an increase in Lp(a) levels40-42, but others have not43-45 and suggested that the former may have been confounded by diagnostic ascertainment bias and/or unequal distributions of LPA risk alleles between FH and non-FH populations44,45.”

    From Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening (2025) · cites this paper as [40]

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Metadata

Authors
Lingenhel, A., Kraft, H. G., Kotze, M., Peeters, A. V., Kronenberg, F., Kruse, R., & Utermann, G.
Venue
European Journal of Human Genetics
Publisher
Springer Science and Business Media LLC
Published
1998-01
Volume
6
Issue
1
Pages
50-60
ISSN
  • 1018-4813
  • 1476-5438
DOI
10.1038/sj.ejhg.5200152
Cited by
43
References
1
Language
en
Licence
www.springer.com/tdm (tdm)

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