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Elevated Lipoprotein(a) in Perinatally HIV-Infected Children Compared With Healthy Ethnicity-Matched Controls
Malon Van den Hof1, Mirthe J Klein Haneveld1, Charlotte Blokhuis1
1Pediatric Infectious Diseases, Emma Children's Hospital, Amsterdam, the Netherlands.
Insights
Perinatally HIV-infected children on combination antiretroviral therapy show elevated Lipoprotein(a) levels, suggesting a potential increase in cardiovascular disease risk. Further research is needed to confirm this association.
Area of Science:
- Pediatrics
- Cardiology
- Infectious Diseases
Background:
- Cardiovascular disease (CVD) risk in perinatally HIV-infected (PHIV+) patients on combination antiretroviral therapy (cART) is not well understood due to their young age.
- Lipoprotein(a) (Lp(a)) is a known independent causal risk factor for CVD in the general population, but its role in PHIV+ is less established.
Purpose of the Study:
- To compare lipid profiles, specifically Lp(a) levels, between cART-treated PHIV+ children and age/sex-matched controls.
- To investigate associations between Lp(a) levels and disease/treatment-related factors, biomarkers, and neuroimaging outcomes in PHIV+ children.
Main Methods:
- Cross-sectional study comparing lipid profiles (including nonfasting Lp(a)) in 35 cART-treated PHIV+ children (8-18 years) and 37 controls.
- Linear regression models were used to explore associations between Lp(a) and various clinical and biological factors.
Main Results:
- PHIV+ children exhibited significantly higher Lp(a) levels compared to controls (43.6 vs 21.8 mg/dL; P = .033).
- No significant differences were observed in other lipid levels, apolipoprotein B, apolipoprotein CIII, apolipoprotein E, or APOE genotype.
- Higher Lp(a) correlated with higher apoB and lower monocyte chemoattractant protein-1 and triglyceride levels in PHIV+ children, but not with HIV/cART variables or neuroimaging outcomes.
Conclusions:
- cART-treated PHIV+ children demonstrate elevated Lp(a) levels, potentially indicating an increased CVD risk.
- Future studies should examine the relationship between Lp(a) and subclinical/clinical CVD measures in this population.
Background:
HIV-associated cardiovascular disease (CVD) risk in combination antiretroviral therapy (cART)-treated perinatally HIV-infected patients (PHIV+) remains unknown due to the young age of this population. Lipoprotein(a) (Lp(a)) has been established as an independent causal risk factor for CVD in the general population but has not been well established in the population of PHIV+.
Methods:
We cross-sectionally compared lipid profiles, including nonfasting Lp(a), together with total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides between 35 cART-treated PHIV+ children aged 8-18 years and 37 controls who were matched for age, sex, ethnicity, and socioeconomic status. We explored associations between Lp(a) and disease- and treatment-related factors (inflammation, monocyte activation, and vascular), biomarkers, and neuroimaging outcomes using linear regression models.
Results:
PHIV+ children had significantly higher levels of Lp(a) compared with controls (median, 43.6 [21.6-82.4] vs 21.8 [16.8-46.6] mg/dL; P = .033). Other lipid levels were comparable between groups. Additional assessment of apolipoprotein B, apolipoprotein CIII, apolipoprotein E, and APOE genotype revealed no significant differences. Higher Lp(a) levels were associated with higher plasma apoB levels and with lower monocyte chemoattractant protein-1 and TG levels in PHIV+ children. Lp(a) was not associated with HIV- or cART-related variables or with neuroimaging outcomes.
Conclusions:
cART-treated PHIV+ children appear to have higher levels of Lp(a) compared with ethnicity-matched controls, which may implicate higher CVD risk in this population. Future research should focus on the association between Lp(a) and (sub)clinical CVD measurements in cART-treated PHIV+ patients.
Dutch Trial Register Number:
NRT4074.
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