Seven trials were included in the review (n=884 patients). All trials used adequate randomisation. Only two trials had an adequate method of allocation concealment. All trials were double blinded, and used intention-to-treat analyses. Loss to follow-up rates of trials ranged from zero to 17%.
Compared with placebo, significant reductions in total cholesterol were observed for lovastatin (WMD -21.88, 95% CI -30.98 to -12.78; two trials) and pravastatin (WMD -39.82, 95% CI -74.80 to -4.84; two trials). Significant heterogeneity was found for both outcomes (I2=61% and I2=97%).
Compared with placebo, significant reductions in LDL cholesterol was observed for lovastatin (WMD -25.72; 95% CI -36.40 to -15.05; two trials) and pravastatin (WMD -43.10, 95% CI -69.85, to -16.35; two trials). Significant heterogeneity was found for both outcomes (I2=70% and I2=94%). There were no significant differences in high-density lipoprotein cholesterol between the treatment and placebo groups.
The evidence on target values for LDL cholesterol levels in children was limited to one study that demonstrating that 60% of the children in the treatment group reached the target LDL cholesterol level of less than 130mg/dL. None of the children in the placebo group reached this target LDL cholesterol level.
The evidence of the effect of statins on surrogate markers of atherosclerosis (carotid intima-media thickness, flow-mediated dilation) was limited to two studies. Further results were reported, as were adverse events.