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Hyperlipidemia in Childhood. Radha R. Cohen, M.D., F.A.A.P Pediatric Grand Rounds April 1, 2004. Hyperlipidemia in Childhood Overview. Basic lipoprotein structure and metabolism Role of childhood hyperlipidemia in atherosclerosis Classification of hyperlipidemias

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hyperlipidemia in childhood

Hyperlipidemia in Childhood

Radha R. Cohen, M.D., F.A.A.P

Pediatric Grand Rounds

April 1, 2004

hyperlipidemia in childhood overview
Hyperlipidemia in ChildhoodOverview
  • Basic lipoprotein structure and metabolism
  • Role of childhood hyperlipidemia in atherosclerosis
  • Classification of hyperlipidemias
  • Pediatric cholesterol screening guidelines
  • Management of hyperlipidemia in children
hyperlipidemia in childhood definition
Hyperlipidemia in ChildhoodDefinition

Hyperlipidemias = group of metabolic disorders characterized by an abnormal accumulation of various lipids in plasma. This may be due to genetics, diet or other acquired factors.

Cholesterol and trigylceride are the primary lipids in plasma. Because they are insoluble in plasma, they are transported within the vascular space as lipoproteins.

hyperlipidemia in childhood lipoprotein structure
Hyperlipidemia in ChildhoodLipoprotein structure

Lipoprotein structure

  • hydrophobic core
    • triglyceride and/or
    • cholesterol ester
  • surface coat
    • phospholipid monolayer
    • interspersed free cholesterol and apolipoproteins
hyperlipidemia in childhood 4 major classes of lipoproteins
Hyperlipidemia in Childhood4 Major Classes of Lipoproteins

Lipoproteins are divided into several classes based on their density.

Each class appears to have distinct functions and atherogenic risk.

hyperlipidemia in childhood classes of lipoproteins
Hyperlipidemia in Childhood Classes of Lipoproteins
  • Total Cholesterol measured in the blood or serum can be viewed as the sum of cholesterol carried in the different major lipoproteins:
    • LDL-cholesterol
    • HDL-cholesterol
    • VLDL-cholesterol
hyperlipidemia in childhood ldl
Hyperlipidemia in Childhood LDL

LDL-cholesterol makes up the majority (60-70%) of cholesterol in the blood.

It has B-100 as its major apolipoprotein; lipoproteins that contain B-100 accumulate in arteries and within atherosclerotic plaques.

It is viewed as the atherogenic lipid; high levels in adults have been correlated with coronary artery disease.

hyperlipidemia in childhood ldl8
Hyperlipidemia in Childhood LDL

LDL-cholesterol receptors are present throughout the body and their metabolism is highly regulated by intracellular cholesterol levels.

Brown and Goldstein received the Noble prize in 1985 for their work elucidating the control and metabolism of LDL-receptors.

hyperlipidemia in childhood hdl
Hyperlipidemia in Childhood HDL

HDL-cholesterol typically makes up 20-25% of the total cholesterol.

It is involved with transport of surplus cholesterol out of the tissue; this reverse transport may be responsible for its protective action against atherosclerosis.

In populations with elevated LDL, HDL-levels are inversely correlated with coronary atherosclerosis.

hyperlipidemia in childhood vldl and chylomicrons
Hyperlipidemia in Childhood VLDL and Chylomicrons

These are the largest of the lipoproteins and are major carriers of triglycerides (TG).

TG are the main storage form of fatty acids. Long chain fatty acids are absorbed in the intestine and combine to form triglycerides and are transported through the thoracic duct to enter the blood stream as chylomicrons.

Chylomicrons are cleared from the blood stream after fasting by lipoprotein lipase.

hyperlipidemia in childhood atherosclerosis
Hyperlipidemia in ChildhoodAtherosclerosis

Clear evidence linking abnormalities in lipid and lipoprotein levels to premature atherosclerosis.

Studies in adults show an unequivocal relationship of elevated levels of total cholesterol and LDL-C to premature atherosclerosis.

atherosclerosis and coronary artery disease
Atherosclerosis and Coronary Artery Disease
  • Atherosclerosis is a disease of large arteries that causes deposits of yellowish plaques containing lipoid material and cholesterol in the intima of vessel walls.
  • This is the pathogenic mechanism for coronary and peripheral vascular disease in adults.
atherosclerosis and coronary artery disease13
Atherosclerosis and Coronary Artery Disease
  • Advanced lesion results from:
    • proliferation of smooth muscle cells and macrophages
    • formation of collagen matrix by smooth muscle
    • accumulation of lipid within the cells and surrounding tissue
atherosclerosis begins in childhood
Atherosclerosis Begins in Childhood
  • In 1962, Strong and McGill reported the autopsy findings of >500 subjects ages 1-69 yrs
  • Fatty streaks rare in 1st decade of life but almost universal by age 20 yrs
progression of atherosclerosis
Progression of Atherosclerosis
  • In Strong & McGill’s study, fibrous plaques were 1st observed in the second decade but increased in frequency and extent during the 3rd & 4th decades.
atherosclerosis and cad
Atherosclerosis and CAD
  • Later in life, fibrous plaques may occlude the vessel lumen and potentiate thrombus formation.
hyperlipidemia in childhood cad begins in childhood
Hyperlipidemia in ChildhoodCAD Begins in Childhood
  • Clinical sequelae of atherosclerosis do not generally occur until later in life.
  • However, there is significant evidence that the pathologic changes begin years prior and are linked to childhood cholesterol levels.


cholesterol levels in childhood and atherosclerosis
Cholesterol Levels in Childhood and Atherosclerosis
  • Bogalusa Heart Study:
  • children who had their coronary risk factors measured sequentially as participants in this study and then died accidentally were studied at autopsy
  • extent of fatty streaks was related to total and LDL cholesterol
  • fatty streaks in coronaries related best to VLDL
  • inverse relationship of fatty streaks to HDL
cholesterol levels in adolescence linked to atherosclerosis
Cholesterol Levels in Adolescence Linked to Atherosclerosis
  • PDAY (Pathological Determinants of Atherosclerosis in Youth) Study- ongoing autopsy study of progression of atherosclerosis in subjects 15-34yrs
  • VLDL and LDL positively and HDL negatively associated with fatty streaks and fibrous plaques
  • Raised lesions were found in those as young as 25yrs
cholesterol levels in childhood and cad in adulthood
Cholesterol Levels in Childhood and CAD in Adulthood
  • Epidemiological investigations provide further evidence of the importance of cholesterol levels in pediatrics
  • Cross-population studies show children from countries with high incidence of CAD in adulthood have higher cholesterol levels than their counterparts in countries with low incidence of CAD
  • Within a population, elevated levels of total and LDL cholesterol in children have been associated with CAD in adult relatives
hyperlipidemia in childhood summary of data
Hyperlipidemia in Childhood Summary of Data
  • Evidence demonstrates that:
    • fatty streaks occur in young people and then progress to atherosclerotic plaques
    • extent of arterial lesions is related to serum lipid (cholesterol) levels
    • manipulation of cholesterol levels can affect development of atherosclerosis
    • therefore...
  • Efforts to prevent the development and progression of atherosclerosis should begin in childhood and adolescence.

Hyperlipidemia in ChildhoodGoal of the Pediatrician

  • Goal of detection / treatment...
    • prevention of premature coronary artery disease
  • Foundation of this goal depends on...
    • coronary artery disease begins in childhood
    • coronary artery disease is related to blood cholesterol levels
    • lowering cholesterol in children will be effective in  CAD
national cholesterol education program ncep
National Cholesterol Education Program (NCEP)
  • The NCEP was created by the National Heart, Lung, and Blood Institute of the NIH in 1985.
  • Its charge was to reduce the prevalence of hypercholesterolemia in the US population and thereby reduce the morbidity and mortality associated with CAD.
hyperlipidemia in childhood definition s
Hyperlipidemia in ChildhoodDefinitions
  • Hypercholesterolemia =
    • total-C or LDL-C  95th % for age
  • Hypertriglyceridemia =
    • TG  95th % for age
  • These are working definitions of hyperlipidemia
  • Levels associated with the least risk of developing CAD in adulthood have not been determined
hyperlipidemia in childhood normal values
Hyperlipidemia in ChildhoodNormal Values

National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents

hyperlipidemia in childhood normal values26
Hyperlipidemia in ChildhoodNormal Values

National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents

hyperlipidemia in childhood classification
Hyperlipidemia in ChildhoodClassification:
  • Primary versus Secondary
    • first consideration - whether the hyperlipidemia is primary (genetic dyslipidemias) or secondary to a metabolic disease or exogenous cause
    • common secondary causes during infancy
      • glycogen storage disease and biliary atresia
    • common secondary causes in childhood
      • hypothyroidism, diabetes, nephrotic syndrome
    • common exogenous causes
      • oral contraceptives, alcohol, steroids
hyperlipidemias secondary causes
HyperlipidemiasSecondary Causes




Steroid therapy

Endocrine and Metabolic

Acute intermittent prophyria

*Diabetes mellitus





Storage disease

Cystine storage disease

Gaucher disease

*Glycogen storage disease

Juvenile Tay-Sachs disease

Niemann-Pick disease

Tay-Sachs disease


Chronic renal failure

Hemolytic-uremic syndrome

*Nephrotic syndrome


Benign recuurent intrahepatic cholestasis

*Congenital biliary atresia

Acute and transient




Anorexia nervosa

Idiopathic hypercalcemia

Klinefelter syndrome


Systemic lupus erythematosus

Werner syndrome

KwiterovichP:Disorders of lipid metabolism, in Rudolph AM (ed): Pediatrics, ed 17.

hyperlipidemia in childhood frederickson classification
Hyperlipidemia in ChildhoodFrederickson Classification

In Circulation 1965, Frederickson and Lees published a description of 5 phenotypes to categorize people with familial hyperlipidemia according to their pattern of elevation of plasma lipoproteins.

As knowledge progressed, it has become apparent that there may be several different genetic and secondary causes of the same Frederickson phenotype.

This classification system has now fallen out of use.

clinically important genetic dyslipidemias
Clinically Important Genetic Dyslipidemias
  • For clinical purposes, the following categories are more useful in determining risk of atherosclerosis, and planning treatment:
    • Hypercholesterolemia
    • Combined hyperlipidemia
    • Hypoalphalipoproteinemia
  • Defined as total cholesterol >170mg/dL for children ages 2-19 yrs
  • An isolated elevation of cholesterol is nearly always due to increase in LDL-C
  • 2 genetic disorders are assoc. with

Total-C & LDL-C = 2-5Xnormal

-familial hypercholesterolemia

-familial defective apoB-100

  • Familial hypercholesterolemia is caused by a mutation in LDL receptor gene on short arm of chromosome 19.
  • Familial defective apoB-100 is due to rare mutations of the apoB gene.
  • In both cases, LDL receptors are unable to interact with apo-B, the protein ligand on LDL particles.
  • Both have autosomal dominant pattern of inheritance.
familial hypercholesterolemia
Familial Hypercholesterolemia
  • Most commonly recognized form of familial hyperlipidemia in childhood
  • Incidence of heterozygotes is 1:500 and homozygotes 1: 1 million
  • Homozygotes present in childhood with serum cholesterol between 400-800mg/dL and cutaneous and tendon xanthomas. Angina and MI before adolescence are common, and most have severe CAD by age 30. Aortic stenosis is also seen.
tendon xanthomas
Tendon Xanthomas

tendon xanthomas of the achilles and elbow

tendon xanthomas36
Tendon Xanthomas

tendon xanthomas of the hand

familial hypercholesterolemia findings in homozygotes
Familial Hypercholesterolemia Findings in Homozygotes

left coronary artery narrowing

supravalvar lipid deposition

eye findings in familial hypercholesterolemia
Eye Findings in Familial Hypercholesterolemia

Early corneal arcus

Cholesterol deposits in retinal fundus

familial hypercholesterolemia heterozygous form
Familial HypercholesterolemiaHeterozygous Form
  • LDL-C is > 95% at birth.
  • Lipid levels remain markedly elevated throughout childhood and adulthood with total cholesterol ~300-400mg/dL and LDL-C ~200-300mg/dL.
  • Clinical manifestations include tendon xanthomas after age 20, early corneal arcus, and CAD after age 30.
  • This diagnosis should strongly be suspected in anyone with high LDL-C and tendon xanthomas in the patient or 1st degree relatives.
familial hypercholesterolemia and cad
Familial Hypercholesterolemiaand CAD
  • In heterozygous males, the risk for development of CAD is estimated to be 20% at age 40yrs, 45% at age 50yrs, and 75% at age 60yrs.
  • FH is thought to account for 3% of premature CAD in the US.
familial hypercholesterolemia42
Familial Hypercholesterolemia
  • Family history and screening of family members should reveal 1/2 of 1st degree relatives with FH
  • Diagnosis can be confirmed by measuring LDL receptor activity in cultured skin fibroblasts or identifying the gene mutation.
  • Prenatal diagnosis is possible by assessing LDL receptor activity in cultured amniotic cells.
  • Genetic counseling is important, especially if partner’s cholesterol is elevated or not known.
combined hyperlipidemia
Combined Hyperlipidemia
  • Familial combined hyperlipidemia was 1st described by Goldstein et al. as dominantly inherited hyperlipidemia and CAD.
  • Affected individuals have either TG or LDL-C >90% or both TG & LDL-C >90%.
  • Phenotype may vary among family members or even from time to time in same individual. Presentation usually delayed until 3rd decade of life. No cutaneous or ocular findings.
  • Thought to affect ~1% of population and account for 10% of premature CAD.
  • Defined as HDL-C < 10% for age and sex associated with normal LDL-C and TG levels.
  • Appears to have autosomal dominant pattern of inheritance in that ~1/2 of family members have low HDL-C and premature atherosclerosis.
  • No clinical manifestations other than premature atherosclerosis with CAD common as early as 4th decade.
cholesterol screening in children
Cholesterol Screening in Children
  • The NCEP recommended selective screening of children and adolescents, targeting those who were likely to become adults with high blood cholesterol and who would thus be at an increased risk for the development of cardiovascular disease.
cholesterol screening
Cholesterol Screening
  • Reasoning for selective screening
    • children and adolescents with elevated blood cholesterol (particularly LDL) frequently come from families in which there is a high incidence of CAD among adult members
    • high blood cholesterol aggregates in families as a result of both shared environments and genetic factors
    • major risk factor for hypercholesterolemia in a child is a family history of premature CAD or hypercholesterolemia
cholesterol screening47
Cholesterol Screening
  • NCEP did not recommend universal screening (controversial)
  • Reasons against universal screening:
  • quite a few children with high cholesterol will not have high enough levels as adults to require treatment
  • leads to many young people inappropriately labeled as having “disease”
  • could lead to overuse of cholesterol-lowering drugs in children
cholesterol screening48
Cholesterol Screening
  • Reasons for recommending universal screening:
  • ~50% of children with elevated cholesterol levels would be missed
  • universal screening may benefit young parents as well
  • children are more likely to receive regular health care than young adults

Cholesterol Screening

  • Selective screening approach
    • based on detailed family history and assessment of concomitant risk factors
    • makes it possible to identify a high risk subset while providing a reasonable balance between the number to be tested and the number to be detected
selective cholesterol screening
Selective Cholesterol Screening

Who should be screened?

  • Children and adolescents with:

-family history of premature atherosclerosis (parents or grandparents with MI, angina pectoris, peripheral vascular disease, cerebrovascular disease, or sudden cardiac death at or before age 55yrs)

-parent with high cholesterol (>240mg/dL)

-unknown family history, especially those with other risk factors (hypertension, diabetes, obesity, smoking)

age for cholesterol screening
Age for Cholesterol Screening
  • When do you screen?
    • Anytime after 2 years of age
      • cholesterol levels relatively stable by this time
      • no treatment recommendations for children less than 2 years old
    • If levels acceptable, repeat after 5 years
cholesterol screening52
Cholesterol Screening
  • What do you order?
    • Total Blood Cholesterol
      • less expensive, random/nonfasting
    • Fasting Lipid Profile
      • 12 hour fast
      • measure total cholesterol, HDL, TG
      • LDL estimated by formula from Lipid Research Clinics:
        • LDL = total cholesterol - (TG/5 + HDL)
        • inaccurate if TG > 400 mg/dl or if not fasting
cholesterol screening53
Cholesterol Screening
  • What to measure also depends on reason for screening
      • parental high cholesterol  total cholesterol
      • family history of CAD  fasting lipid profile
    • LDL level determines risk and need for treatment
cholesterol screening55
Cholesterol Screening
  • If LDL-C <110 mg/dL, no further testing.
  • If LDL-C 110-129 mg/dL,educate family, prescribe “Step One” diet, and recheck in 1 year.
  • If LDL-C >130 mg/dL, evaluate for causes (r/o secondary causes like hypothyroidism, diabetes; if familial suspected, measure lipid profiles of family) and begin treatment.
management of elevated cholesterol
Management of Elevated Cholesterol
  • LDL-C>130 mg/dL
    • Start “Step One” Diet
  • Recheck level in 6 wks.
  • If LDL not <110 mg/dL, intensify “Step One” Diet and recheck in 3 months.
  • If goal still not met, prescribe “Step Two” diet for next 3 months.
  • If goal still not met after 1 yr with diet alone, consider pharmacotherapy.
hyperlipidemia in childhood detection and treatment
Hyperlipidemia in ChildhoodDetection and Treatment

long term monitoring = recheck lipoprotein analysis 2x / year

diet therapy
Diet Therapy
  • Primary approach to treating children and adolescents with elevated cholesterol levels
  • Aim of diet therapy is to reduce elevated blood cholesterol levels while maintaining a nutritionally adequate eating pattern
  • It is prescribed in two steps that progressively reduce the saturated fatty acid (SFA) and cholesterol intake
diet therapy59
Diet Therapy
  • Step One diet
      • < 30% total calories from fat
      • < 10% total calories from SFA
      • < 300 mg/day cholesterol
      • adequate calories for growth and development
  • Requires detailed assessment of current eating patterns and instruction by a physician, RD, or other professional
diet therapy60
Diet Therapy
  • Step Two diet
    • prescribed if careful adherence to Step One diet for at least 3 months fails to achieve the minimal goals of therapy
    • further reduction of SFAs and cholesterol
      • < 30% calories from fat (SAME as Step One)
      • < 7% total calories from SFA
      • < 200 mg/day cholesterol
diet therapy61
Diet Therapy

National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents

mg of cholesterol in foods
bacon, 3 slices = 16 mg

chicken (3.5 oz), lt meat, no skin=75 mg

shrimp (3.5 oz) = 195 mg

egg, yolk = 213 mg

cheddar cheese (1 oz) = 30 mg

bread, one slice = 0 mg

butter (one TBS) = 31 mg

margarine (one TBS) = 0 mg

McDonald’s Big Mac = 100 mg

McDonald’s Egg McMuffin = 235 mg

Pizza Hut Pan Pizza (1 slice) = 25 mg

potato chips (1 oz) = 0 mg

cola, regular = 0 mg

chocolate chip cookies(4) =18mg

peanuts (1 oz) = 0 mg

Mg of Cholesterol in Foods

cholesterol ( 300 mg/day)

diet therapy63
Diet Therapy
  • General food guidelines
    • meat, poultry, and fish
      • major sources of high quality protein
      • but also major contributors of SFA, total fat, and cholesterol
      • use LEAN meat, remove skin from poultry
    • eggs
      • good source of high quality protein, iron, vits
      • yolks very high in cholesterol (whites=none)
      • 2 egg whites substituted for 1 egg in recipes
diet therapy64
Diet Therapy
  • Fats and oils
    • intake of saturated oils: coconut, palm kernel, palm
    • intake of unsaturated oils: sunflower, corn, canola, olive, peanut
    • margarine instead of butter (with unsaturated oil listed as first ingredient)
diet therapy65
Diet Therapy
  • Plant stanol esters
    • Are available in low-fat margarine spreads
    • Also available in salad dressings and snack bars
    • Structurally stanol esters are similar to cholesterol and inhibit cholesterol absorption in the gut by competitive mechanisms
plant sterol esters
Plant Sterol Esters
  • Studies have demonstrated that consumption of low-fat margarine containing stanol esters can lower total and LDL cholesterol by 10-15% in hypercholesterolemic subjects
  • Have been studied in children with no adverse clinical effects noted
  • Does not affect HDL-C or TG levels
  • Effects on Total and LDL-C seen in 4-8 weeks with a daily dose of 2-3 g (~3 Tbsp of the commercially available products)
  • Examples: Benecol and Take Control
  • In addition to diet prescription, don’t forget to recommend regular aerobic exercise
  • 30-45 minutes, at least 4-5 times a week
  • Can increase HDL-C
  • Can help with regards to other risk factors for CAD, such as obesity and hypertension
drug therapy
Drug Therapy
  • Only a small proportion of children should be considered for drug treatment because of the
    • potential side effects
    • relative expense of medications
    • lack of definitive, prospective data on the effect of such treatment on children
drug therapy69
Drug Therapy
  • Consider drug therapy
    • following adequate trial of diet therapy for 6 months to 1 year if
      • LDL remains > 190 mg/dl
      • LDL remains > 160 mg/dl and
        • + family history of premature CAD or
        • 2+ other risk factors still exist (HDL<45 mg/dl, obesity, diabetes, hypertension)
      • LDL > 130 mg/dl but <160 mg/dl, no specific recommendations for drug therapy
drug therapy70
Drug Therapy
  • Only approved for children older than 10 years of age
  • Diet & exercise therapy must continue
  • Follow up
    • 6 weeks after starting medication
    • every 3 months thereafter until goal is met
    • then every 6 months
drug therapy71
Drug Therapy
  • Bile-acid binding resins
  • Ezetimibe
  • HMG-CoA reductase inhibitors (“statins”)
  • Niacin (nicotinic acid)
  • Fibric acid derivatives
bile acid sequestrants
Bile Acid Sequestrants

Primary therapy recommended in children

Cholestyramine (Questran) and colestipol (Cholestid)

Reduce LDL levels by ~20%

Long-term compliance limited, presumably due to unpalatability and GI side effects (nausea, bloating, constipation, flatulence)

bile acid sequestrants73
Bile Acid Sequestrants
  • Mechanism of action:
    • anion exchange resins
    • bind (-) bile acids in SI
    • resin/bile complex out via feces
    • prevents enterohepatic circulation of bile acids
    •  bile acid concentration in hepatocytes causes an  conversion of cholesterol to bile acids
    • causes  in intracellular cholesterol
    • activates an increased uptake of LDL cholesterol particles
    • outcome =  plasma cholesterol
bile acid sequestrants74
Bile Acid Sequestrants

Overall safe because not absorbed and lack systemic toxicity

However, they can cause malabsorption of fat-soluble vitamins and folic acid so a daily MVI containing folic acid and iron is recommended

Their use is limited in patients who also have elevated TG since they can increase TG levels

Check CBC and LFTs annually in patients

bile acid sequestrants75
Bile Acid Sequestrants
  • cholestyramine and colestipol
    • both are powders that are mixed with water or juice before ingestion; cholestyramine is also available as flavored bars
    • choice of one over the other depends on individual taste preference and side effects
    • dose is not related to body weight but to levels of total and LDL cholesterol
      • start on lowest dose possible, then  one dose at a time until goal achieved
bile acid sequestrants76
Bile Acid Sequestrants
  • cholestyramine and colestipol
    • dosing regimen
      • one dose = 9 g packet of cholestryramine, one bar of cholestyramine, or 5 g colestipol
      • daily doses TC LDL

1 <245 <195

2 245-300 195-235

3 301-345 236-280

4 345

      • take immediately before, during, or after meals (largest amount of bile acids in intestine)
ezetimibe zetia
Ezetimibe (Zetia)
  • Relatively new agent
  • Inhibits intestinal absorption of cholesterol
  • Limited study in children 10-18 yrs
  • Lowers LDL-C by up to 15-20%
  • May decrease TG and increase HDL-C
  • Given as a single 10mg dose tablet
  • No major side effects noted
  • In adults has been used in conjunction with statins
  • HMG-CoA reductase inhibitors work by inhibiting the rate-limiting step in cholesterol biosynthesis
  • Have been used in adults >10-15 years with good success and safety
  • Can decrease Total and LDL-C by 20-60%
  • Limited studies in children show efficacy and no significant side effects, but studies were underpowered for safety
  • Must monitor LFTs every 3-6 months as there is a potential for hepatocellular toxicity
  • Also, statins are potentially teratogenic so they should be used with caution in female adolescents.
hyperlipidemia in childhood summary
Hyperlipidemia in ChildhoodSummary
  • CAD is a major cause of significant mortality, morbiditity, and expense
  • It begins in childhood and progresses in severity as we age
  • It results from a combination of inter-related factors such as genetics, hypercholesterolemia, hypertension, obesity, diabetes, and smoking
  • Many of these risk factors are largely preventable and/or modifiable
hyperlipidemia in childhood summary81
Hyperlipidemia in ChildhoodSummary
  • Efforts to prevent the development and progression of atherosclerosis should begin in childhood and adolescence
  • Selective cholesterol screening can identify those children at highest risk for hypercholesterolemia
  • For those children with hypercholesterolemia, a diet low in SFAs and cholesterol is the mainstay of therapy