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Apolipoprotein (a) phenotypes and lipoprotein (a) concentrations in patients with type III hyperlipoproteinaemia
G Feussner1, V Feussner, R Ziegler
1Department of Internal Medicine I (Endocrinology and Metabolism), University of Heidelberg, Germany.
Insights
Lipoprotein (a) [Lp(a)] levels and apolipoprotein (a) [apo(a)] phenotypes were studied in type III hyperlipoproteinaemia (HLP). Results indicate apo(a) polymorphism does not significantly influence type III HLP expression.
Area of Science:
- Cardiovascular genetics
- Lipid metabolism disorders
- Atherosclerosis pathogenesis
Background:
- Familial hyperlipoproteinaemia type III (HLP) significantly increases atherosclerosis and cardiovascular disease (CVD) risk.
- Considerable individual variation exists in CVD susceptibility among HLP patients.
- The role of lipoprotein (a) [Lp(a)] in HLP pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the potential influence of Lp(a) on the pathogenesis of type III HLP.
- To determine if Lp(a) concentrations or apo(a) phenotypes correlate with type III HLP.
Main Methods:
- Determined apolipoprotein (a) [apo(a)] phenotypes and Lp(a) concentrations in 76 type III HLP patients and 76 controls.
- Compared Lp(a) levels and apo(a) phenotype frequencies between HLP patients and healthy controls.
- Utilized data from a university out-patient lipid disorder clinic.
Main Results:
- Lp(a) concentrations were not significantly different between type III HLP patients (14.1 ± 19.1 mg/dL) and controls (13.3 ± 16.2 mg/dL).
- No significant difference was observed in apo(a) phenotype frequencies between the HLP group and the control group.
- P-value for Lp(a) difference was 0.549 (NS); P-value for phenotype difference was > 0.1.
Conclusions:
- Apolipoprotein (a) [apo(a)] polymorphism does not appear to significantly contribute to the phenotypical expression of type III hyperlipoproteinaemia (HLP).
- The findings suggest that Lp(a) is unlikely to be a major factor in the development of type III HLP.
- Further research may explore other genetic or environmental factors influencing CVD risk in type III HLP.
Objectives:
The familial lipoprotein disorder type III hyperlipoproteinaemia (HLP) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation amongst affected individuals in their susceptibility to cardiovascular disease (CVD). Therefore, it was the aim of our study to investigate the possible influence of lipoprotein (a) [Lp(a)] in the pathogenesis of type III HLP:
Design:
Apolipoprotein (a) [apo(a)] phenotypes and Lp(a) concentrations were determined in patients with the disease and in an appropriate control group.
Setting:
University out-patient lipid disorder clinic.
Subjects:
Seventy-six apoE-2 homozygous patients with type III HLP and 76 normolipidaemic and healthy age- and sex-matched controls.
Main Outcome Measures:
The frequencies of different apo(a) phenotypes and their correlations with Lp(a) serum concentrations were determined in patients and controls.
Results:
Lp(a) concentrations were not significantly different in type III HLP patients (14.1 +/- 19.1 mg dl-1) as compared with the controls (13.3 +/- 16.2 mg dl-1; P = 0.549, NS). In addition, there was no significant difference in apo(a) phenotype frequencies amongst both groups (0.2 > P > 0.1).
Conclusions:
We conclude that the apo(a) polymorphism does not participate (to a significant extent) in the phenotypical expression of type III HLP: