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Updated: Aug 5, 2026

On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Increased inflammatory markers in children with familial hypercholesterolaemia
T Ueland1, M N Vissers, A Wiegman
1Research Institute for Internal Medicine, Section of Endocrinology, Rikshospitalet, University of Oslo, Norway. thor.ueland@medisin.uio.no
Insights
Children with familial hypercholesterolaemia (FH) show higher inflammation markers like neopterin and hsCRP. Statins had minimal impact on these markers in FH children, unlike in adults.
Area of Science:
- Pediatric Cardiology
- Inflammation Research
- Genetic Lipid Disorders
Background:
- Limited data on inflammatory markers in pediatric hypercholesterolemia.
- Investigating inflammation in children with heterozygous familial hypercholesterolaemia (FH).
- Assessing neopterin, hsCRP, and sCD40L levels in FH children.
Purpose of the Study:
- To determine the extent and nature of inflammation in children with FH.
- To compare inflammatory markers in FH children versus their unaffected siblings.
- To evaluate the impact of pravastatin treatment on these markers.
Main Methods:
- Compared inflammatory marker concentrations in 207 FH children and 84 healthy siblings.
- Measured serum neopterin, hsCRP, and sCD40L.
- Assessed the effect of 2-year pravastatin or placebo treatment.
Main Results:
- FH children had significantly higher neopterin and hsCRP levels than siblings.
- sCD40L levels did not differ between groups.
- Pravastatin reduced neopterin but not other markers, with no significant difference from placebo.
Conclusions:
- Findings suggest low-grade monocyte/macrophage activation in early atherogenesis in FH children.
- Inflammation and statin's anti-inflammatory effects appear less pronounced in FH children than adults.
- Highlights differences in inflammatory profiles between pediatric and adult FH.
Background:
While data are abundant on increased levels of inflammatory markers in adult patients with hypercholesterolaemia, such data in children are limited. Therefore, we sought to investigate the degree and character of inflammation in children with heterozygous familial hypercholesterolaemia (FH) by measuring levels of neopterin, high-sensitivity C-reactive protein (hsCRP), and soluble CD40 ligand (sCD40L).
Materials And Methods:
In the present study, we compared the concentration of inflammatory markers in children suffering from heterozygous FH (n = 207) with those in unaffected siblings (n = 84). Furthermore, we investigated the effect of 2-year treatment with pravastatin (20-40 mg qd) or placebo on plasma levels of those markers.
Results:
Our main finding was that serum levels of neopterin and hsCRP were significantly higher in FH children compared with healthy siblings, whereas sCD40L was not. Body mass index and high-density lipoprotein cholesterol levels were significant independent predictors of hsCRP and neopterin. Furthermore, pravastatin therapy decreased neopterin, but not hsCRP and sCD40L, in the FH children, but these changes were not different from the placebo group.
Conclusion:
These findings indicate low-grade monocyte/macrophage hyperactivity in the early stages of atherogenesis, but our findings also suggest that inflammation as well as anti-inflammatory effects of statins are less prominent features of atherosclerosis in FH children than in FH adults.
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