**4. Dyslipidemia**

Dyslipidemia is a known risk factor for atherosclerosis and should be identified in youth to intervene in time and to reduce not only future CVD disease [19], but also arterial ischemic stroke in children, where dyslipidemia and hypertriglyceridemia were found to be more prevalent [20].

Commonly, lipid screening includes measurement of total cholesterol, highdensity lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL) and triglycerides. Additionally, several other lipoproteins, such as apolipoprotein A1 and B can be evaluated and provide further information on cardiovascular risk.

The prevalence of dyslipidemia is increasing due to increasing obesity, where almost in a half of children with obesity, a type of dyslipidemia (hypertriglyceridemia, lowered HDL, elevated LDL) is present [21]. School children, who are overweight, are 2.4 to 7.1 more likely to have elevated total cholesterol, LDL and triglycerides in comparison to lean peers [22].

Dyslipidemia in children can be a consequence of inherited dyslipidemia syndrome. Familial hypercholesterolemia, a monogenic, autosomal dominant disorder, is caused by mutations of LDL receptor or other protein that affects LDL receptor activity. Homozygous forms are rare, but are associated with rapidly progressive atherosclerosis leading to CVD and mortality in the first two decades of life. More commonly, heterozygous form is present with accelerated atherosclerosis and cardiovascular events before age of 50 years. These patients mostly have isolated elevation of LDL [19].

#### *Cardiovascular Risk Factors in Children DOI: http://dx.doi.org/10.5772/intechopen.99729*

Familial combined hyperlipidemia is characterized by mixed dyslipidemia (LDL and triglycerides may be high or normal, HDL normal or reduced) with significant production of very low-density lipoprotein (VLDL) cholesterol and increased risk for CVD. It is less likely to be diagnosed in children, since significant elevations in fats may not occur until late adolescence, however apolipoprotein B levels may rise earlier and may be a better marker for this condition. In adults it is associated with features of metabolic syndrome and insulin resistance [19].

Rarely, severe hypertriglyceridemia may also be of genetic origin. Patients are likely to have a defect in lipoprotein lipase [19].

Some forms of secondary dyslipidemia (**Table 2**) are more frequent in children than in adults, and should be evaluated for [19].

Correction of secondary causes should normalize lipid levels, if there is no underlying genetic factor. Otherwise, the core management of dyslipidemia is lifestyle change with regular exercise, reduced screen time and diet. Dietary change should include total fat in less than 30% of daily caloric intake, with 8–10% saturated fat, avoidance of trans-fats and cholesterol intake less than 300 mg/day. This may be advanced to restriction of saturated fat less than 7% and cholesterol intake less than 200 mg/day if dyslipidemia persists. This level of restriction was found to be safe for growth and development. Water-soluble fiber and plant sterols may complement the diet. Patients with hypertriglyceridemia should also limit their sugar intake with replacement of simple sugars with complex carbohydrates and increase of omega-3 fatty acid intake [19, 23].

If lifestyle change over 6–12 months is unsuccessful, pharmacological treatment may be added. Statins were shown to be efficacious in children with familial hypercholesterolemia with a good safety profile. In children above 10 years of age,


#### **Table 2.**

*Causes of secondary dyslipidemia in children.*

cholesterol absorption inhibitors may be added as adjunctive therapy. Bile acid sequestrants (cholestyramine, colestipol) also lower cholesterol level, but may have adverse gastrointestinal effects, such as gas, bloating, constipation and cramps, that limit their use and decrease compliance. Fibrates, niacin and orlistat lower triglyceride levels. For some genetic causes, novel treatment options are emerging, such as PCSK9 monoclonal antibody therapy [19, 23, 24].
