Statin therapy and secretory phospholipase A₂ in children with heterozygous familial hypercholesterolemia

详细信息    查看全文

• 作者：Marjet J.A.M. Braamskamp ; Sotirios Tsimikas ; Albert Wiegman ; John J.P. Kastelein ; Barbara A. Hutten
• 关键词：Secretory phospholipase A2 ; Familial hypercholesterolemia ; Lipoproteins ; Statins
• 刊名：Atherosclerosis
• 出版年：2013
• 出版时间：August, 2013
• 年：2013
• 卷：229
• 期：2
• 页码：404-407
• 全文大小：247 K

文摘

Objective

Secretory phospholipase A₂ (sPLA₂) enzymes are thought to contribute to atherosclerosis. In this study we assessed levels of sPLA₂ mass and activity, and their relationship to baseline characteristics of children with familial hypercholesterolemia (FH). Furthermore, we evaluated the effect of two years of pravastatin therapy on sPLA₂ levels.

Methods and results

sPLA₂-IIA mass and sPLA₂ activity were measured at baseline and after two years in 187 children with FH (aged 8-18 years) randomized to pravastatin or placebo. At baseline, median [IQR] sPLA₂-IIA mass and sPLA₂ activity levels were 7.2 [5.8-13.2] ng/ml and 36.4 [29.8-47.1] U/ml, respectively. Both sPLA₂-IIA mass and sPLA₂ activity were significantly correlated with high-sensitivity C-reactive protein (r?=?0.33, p?<?0.001 and r?=?0.386, p?<?0 .001, respectively), but not with other cardiovascular risk factors. Baseline levels of sPLA₂-IIA mass and sPLA₂ activity were not significantly associated with carotid intima-media thickness (cIMT) at baseline or at the end of follow-up. After two years, sPLA₂-IIA mass and sPLA₂ activity levels were not significantly reduced in the pravastatin group (p?=?0.20 and p?=?0.63, respectively), nor in the placebo group (p?=?0.17 and p?=?0.11, respectively). Changes from baseline did not differ between the treatment groups for sPLA₂-IIA mass (p?=?0.48) and sPLA₂ activity (p?=?0.88).

Conclusions

sPLA₂-IIA mass and sPLA₂ activity were not significantly associated with cIMT in our pediatric FH cohort. This could indicate that the potential predictive role of sPLA₂ as a biomarker of cardiovascular disease in children with FH is limited. Treatment with pravastatin did not reduce sPLA₂-IIA mass or sPLA₂ activity levels, as compared to placebo. Further studies with larger samples are required to address these issues.