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Dyslipidemias that favor an increased uptake of LDL through the scavenger pathway promote the production of foam cells and their associated atherosclerosis and xanthomas. Apo A-1 is released as a lipid-free protein from the intestine and liver.

Apo A-I is a cofactor for this reaction see Fig. For example, if the TG in HDL are hydrolyzed by hepatic lipase, a smaller HDL particle is produced that is more avidly removed from plasma by cubilin in the kidney. These reactions are part of a process called reverse cholesterol transport. Both these pathways result in delivery of sterol from peripheral tissues and plasma into intestinal cells, promoting the excretion of sterols into the stool.

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Reverse cholesterol transport has been postulated to explain, at least in part, the protective effect that HDL and apo A-I have against the development of atherosclerosis. Conversely, factors that impede this process, such as a dysfunctional HDL, appear to promote atherosclerosis. Clearly, the plasma levels of lipids and lipoproteins result from the influence of a variety of metabolic, genetic, and environmental factors.

In the general population, these levels usually follow a gaussian distribution, often skewed toward higher levels. Similar data are available from such studies as Bogalusa. Human plasma cholesterol levels are lowest during intrauterine life. After 2 years of age, the levels of the lipids and lipoproteins become constant up to adolescence.

As well, in the second decade, the TG are higher than they are in the first decade. This information has important implications for the timing of lipid and lipoprotein screening and the cut points used because lipid concentrations are age and maturation dependent and appear influenced by gender and race as well, albeit to a small degree. Thus, multiple cut points by single age and gender do not appear warranted. Dyslipidemia is present if one or more of these lipid, lipoprotein, or apolipoprotein factors are abnormal. Significant percentages of children and adolescents have elevated concentrations of lipids and lipoproteins.

The Johns Hopkins Textbook of Dyslipidemia

An important epidemiologic aspect of cardiovascular risk in childhood is the tracking of lipid and lipoprotein concentrations over time. Tracking indicates the likelihood that children will maintain their percentile ranking over time and has been demonstrated in a number of studies. The Muscatine investigators also found that onset of obesity in adolescence and young adulthood, cigarette smoking, and use of oral contraceptives may have deleterious effects on adult concentrations of lipids and lipoproteins. Two major approaches have been used to detect dyslipidemia in youth, namely, screening in the general population and in a selected population.

The extensive literature related to these two screening approaches has been reviewed in detail. Lipid screening recommendations have recently been updated by the American Academy of Pediatrics. Traditionally, screening for dyslipidemias in high-risk children has been recommended because of multiple CVD risk factors and a family history of premature CVD or the presence of hypercholesterolemia.

LDL-C has been the main focus of diagnosis and treatment. With obesity, type 2 diabetes, and the metabolic syndrome increasing in the younger population, the focus of screening is likely to be expanded to include other factors, such as obesity, low HDL-C, non—HDL-C TC minus HDL-C , elevated TG, elevated apo B reflecting increased numbers of LDL particles , glucose intolerance and insulin resistance, and higher blood pressure levels. Both the current and evolving concepts in screening for dyslipidemia in youth are discussed. The individualized approach identifies and treats children and adolescents at risk of having high cholesterol levels.

Expanded recommendations of the NCEP Expert Panel on Blood Cholesterol Levels in Children and Adolescents from include performance of selective screening if one of the following conditions is present:. A lipoprotein profile in youth whose parents, grandparents, or siblings required coronary artery bypass graft surgery or percutaneous coronary intervention before the age of 55 years because of premature CAD. A lipoprotein profile in those with a family history of myocardial infarction, angina pectoris, peripheral or cerebral vascular disease, or sudden death before the age of 55 years.

This recommendation might be usefully expanded to a lipoprotein profile in offspring of parents who have any genetically transmissible disorder of lipid metabolism associated with increased atherosclerosis risk, involving elevated LDL-C, non—HDL-C, apo B, TG, low HDL-C, and perhaps Lp a. The NCEP Expert Panel on Blood Cholesterol Levels in Children and Adolescents recommendations from have been modified in the most recent American Academy of Pediatrics statement, which recommends screening of children with a family history of premature CVD or high cholesterol or those for whom a family history is unknown or those with other risk factors for CVD e.

An optimal program would identify individuals at greatest risk for CVD in adulthood; however, there is currently no clinically applicable noninvasive screening tool available to assess this in children without familial hypercholesterolemia. Whereas the current targeted approach based on family history assumes that this information is known, with adult family members information is often not available. Universal lipid screening of all children is controversial. There are a number of advantages and disadvantages of universal screening. What are some of the arguments in favor of universal screening?

Universal screening will undoubtedly detect those with undiagnosed heterozygous FH or more marked FCHL, who will require more intensive treatment, usually drug therapy. This approach might usefully be combined with a case-finding strategy in relatives of patients with FH. Identification of children and adolescents affected with hypercholesterolemia through universal screening may bring to attention their adult relatives who will have greater coronary mortality than relatives of children with normal cholesterol levels.

If universal lipid screening is combined with an assessment of obesity and high blood pressure, this can also lead to the detection of additional relatives from families at high risk for CVD.

Johns Hopkins Textbook Of Dyslipidemia

CVD risk factors cluster in childhood and persist into adulthood. Whereas offspring of parents with CVD generally have higher LDL-C and TG and lower HDL-C in both childhood and young adulthood, the majority of children with dyslipidemia and multiple risk factors will be missed by selective screening.

There are some practical problems with universal screening see later. As well, no longitudinal studies to date are available and are unlikely ever to be available to document that starting lipid treatment in childhood decreases adult CVD. One might argue therefore that universal screening seems all the more urgent, given the epidemic of obesity and the metabolic syndrome in our youth. What are potential concerns about universal lipid screening in childhood?

The use of TC in childhood to predict TC or LDL-C in young adults, sufficiently high to warrant treatment, is often associated with suboptimal sensitivity, specificity, and predictive power of a positive test result. When one uses quantitative traits such as LDL-C values for screening, there is no simple resolution of this problem. A number of longitudinal studies found that when the 75th percentile for TC in children is used as a screening cut point, about half the individuals who will require treatment as adults are identified by universal lipid screening.

In one report, the sensitivity was much lower when screening was performed during adolescence, presumably reflecting the temporary shift of LDL-C to lower values during this period of rapid growth and development. Use of family history information does not substantively improve these results. A combined approach using other CVD risk factors, such as obesity, as part of the screening paradigm for future CVD will probably improve the detection of those adults more likely to develop premature CVD. Health care providers need to be aware of the negative impact of labels on a child. Problems can be created where no problems may have been.

Universal screening raises additional logistic issues. How will pediatricians and family practitioners handle the detection of many children and adolescents with dyslipidemias? Who will counsel in regard to dietary changes, weight loss, and regular exercise habits? Will universal screening, treatment of affected children, and follow-up be cost-effective? Clearly, national resources will be required to change the way pediatric medicine is practiced. For selective screening, a lipoprotein profile after an overnight fast of 10 to 12 hours is measured for screening youth with a positive family history of premature CVD or dyslipidemia or who have obesity, have multiple CVD risk factors, or are suspected of having secondary dyslipidemia.

Levels of lipoproteins are typically measured and expressed in terms of their cholesterol content. Non-HDL and apo B are valid in the nonfasting state. Apo B and apo A-I can also be determined by well-standardized immunochemical methods. Such measurements might provide additional useful information, particularly in youth with premature CAD in their parents. Apo B provides an assessment of the total number of apo B—containing lipoprotein particles.

Advanced lipoprotein testing to determine plasma levels of VLDL, LDL, and HDL subclasses has been performed in children and adolescents by nuclear magnetic resonance spectroscopy or by vertical-spin density-gradient ultracentrifugation in research studies see also later. However, cut points derived from these methods for the diagnosis and treatment of dyslipidemia in youth are currently not available.

However, treatment algorithms in pediatrics are usually focused on fasting LDL-C. TG is usually assessed as part of the dyslipidemic triad and is often elevated in obesity and the metabolic syndrome. Cholesterol levels are reasonably consistent after 2 years of age. Cholesterol levels are not routinely measured before the age of 2 years because no formal treatment is recommended for this age group. Ten years of age range, 9 to 11 years has been proposed as a good time to obtain a standard lipoprotein profile. Children are older and are able to fast easier, the values are predictive of future adult lipoprotein profiles, and puberty has usually not yet started.

In FH heterozygotes, there is a significant fall in the ratio of affected to normal during adolescence. If sampling occurs during adolescence and results are abnormal, levels are likely to be even higher after teenage years. If results during puberty are normal, sampling will need to be repeated toward the end of adolescence 16 years of age for girls and 18 years of age for boys. The complete phenotypic expression of some disorders, such as FCHL, can be delayed until adulthood, and therefore continued evaluation of subjects from high-risk families with FCHL should occur well into adulthood.


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Before a dyslipoproteinemia is considered to be primary, secondary causes must be excluded Table Each child with dyslipidemia should undergo routine blood testing to rule out secondary causes, including a fasting blood glucose concentration and kidney, liver, and thyroid function tests. In secondary dyslipidemia, the associated disorder producing the dyslipidemia should be treated first in an attempt to normalize lipoprotein levels. If an abnormal lipid level persists, for example, as it often does with diabetes mellitus type 1 and nephrotic syndrome, the patient requires dietary treatment and, if indicated, pharmacotherapy with use of the same guidelines as in primary dyslipidemias.

General guidelines for dietary and pharmacologic treatment of primary and secondary dyslipidemias in youth are presented first. Specific therapies relevant to each inherited disorder of dyslipidemia are addressed in subsequent sections of this chapter. The first approach to therapy for children with dyslipidemia is a modified diet containing decreased amounts of total fat, saturated fat, trans -fat, and cholesterol.

The intake of complex carbohydrates is increased, and that of simple sugars is decreased. No decrease in total protein is recommended. Adequate calories should be provided to maintain normal growth and development. Recent data from randomized clinical trials in general populations, such as STRIP, indicate that a diet low in total fat, saturated fat, and cholesterol may be instituted safely and effectively at 6 months of age see also later.

If the dyslipidemia persists i. A Step I diet is usually started, and the lipoprotein profile is rechecked in 6 to 8 weeks. If the dyslipidemia persists, a Step II diet is begun. Both diets require the optimal input of a registered dietitian. This may not always be available, and the health care provider, such as the physician or nurse, may need to provide the basis for the diets in Table along with printed materials that are available from the American Heart Association.

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