Lipid screening and treatment recommendations for children and adolescents.

Pediatric Annals (Impact Factor: 0.29). 07/2012; 41(7):1-10. DOI: 10.3928/00904481-20120625-08
Source: PubMed
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    ABSTRACT: Functional and morphological changes of the arterial wall already present in young children with heterozygous familial hypercholesterolemia (HeFH) suggest that treatment should be initiated early in life to prevent premature atherosclerotic cardiovascular disease. The purpose of this study was to assess the efficacy and particularly safety of statin therapy in children with HeFH. We performed a meta-analysis of randomized, double-blind, placebo-controlled trials evaluating statin therapy in children aged 8 to 18 years with HeFH. Six studies (n=798 children) with 12 to 104 weeks of treatment were included. Total cholesterol, LDL cholesterol, and apolipoprotein B were significantly reduced, whereas HDL cholesterol and apolipoprotein A1 were significantly increased by statin therapy. No statistically significant differences were found between statin- and placebo-treated children with respect to the occurrence of adverse events (RR 0.99; 95% CI: 0.79 to 1.25), sexual development (RR of advancing > or = 1 stage in Tanner classification 0.96; 95% CI: 0.79 to 1.17), muscle toxicity (RR of CK > or = 10 times the upper limit of normal [ULN] 1.38; 95% CI: 0.18 to 10.82), or liver toxicity (RR of > or = 3 times the ULN for ASAT 0.98; 95% CI: 0.23 to 4.26 and for ALAT 2.03; 95% CI: 0.24 to 16.95). We found a minimal difference in growth in favor of the statin group (0.33 cm; 95% CI: 0.03 cm to 0.63 cm). In addition to the fact that statin treatment is efficacious, our results support the notion that statin treatment in children with HeFH is safe. Thus, even though further studies are required to assess lifelong safety, statin treatment should be considered for all children aged 8 to 18 with HeFH.
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    ABSTRACT: Although parent-offspring associations of cardiovascular risk factor variables are known, the age-specific nature of this familial relationship is not clear. This aspect was examined in 727 unrelated children (mean age: 11.2 years) and their parents who participated in the Bogalusa Heart Study during their childhood (mean age: 11.3 years) and adulthood (mean age: 25.5 years). After adjusting for covariates, the mothers' childhood-offspring correlations were consistently higher than mothers' adulthood-offspring correlations for body mass index (BMI) [r = 0.45 vs. 0.32], systolic blood pressure (SBP) [r = 0.30 vs. 0.10], diastolic blood pressure (DPB) [r = 0.22 vs. 0.13] and low-density lipoprotein cholesterol (LDLC) [r = 0.20 vs. 0.11]. In contrast, high-density lipoprotein cholesterol (HDLC) and triglycerides did not show such age-specific trends in mother-offspring correlations. Corresponding father-offspring correlations showed similar patterns, but the differences were of lesser magnitude. Multiple regression analyses using offspring's risk factor variables as dependent variables revealed that parents' childhood obesity, blood pressure and LDLC levels were better predictors of the corresponding variables in the young offspring than parents' adulthood values. Further, sex of either parents or offspring made no difference in the above findings. The magnitude of the familial associations of cardiovascular risk factor variables between parents and offspring are influenced by age. Intrinsic genetic make-up, duration of exposure to environment and gene-environment interactions may play a role in this association.
    Annals of Epidemiology 12/2001; 11(8):522-8. · 2.15 Impact Factor