Download European Atherosclerosis Society (EAS). EAS

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

Pediatric cholesterol screening guidelines

Management of hyperlipidemia in children
Hyperlipidemia in Childhood
Definition
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
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
•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
•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
•LDL-cholesterol makes up the majority (6070%) 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
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
•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
•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
•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 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 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
•FATTY STREAK=>FIBROUS
PLAQUE
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

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


Later in life,
fibrous plaques
may occlude the
vessel lumen and
potentiate
thrombus
formation.
THIS IS WHAT
WE WANT TO
PREVENT!!!
Hyperlipidemia in Childhood
CAD 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




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



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
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

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 Childhood
Goal 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)
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
Definitions

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
National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents
Hyperlipidemia in Childhood
Normal Values
National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents
Hyperlipidemia in Childhood
Classification:

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
·
hypothyroidism, diabetes, nephrotic syndrome
·
oral contraceptives, alcohol, steroids
common secondary causes in childhood
common exogenous causes
Hyperlipidemias
Secondary Causes
Exogenous
Alcohol
Contraceptives
Steroid therapy
Endocrine and Metabolic
Acute intermittent prophyria
*Diabetes mellitus
Hypopituitarism
*Hypothyroidism
Lipodystrophy
Pregnancy
Storage disease
Cystine storage disease
Gaucher disease
*Glycogen storage disease
Juvenile Tay-Sachs disease
Niemann-Pick disease
Tay-Sachs disease
Renal
Chronic renal failure
Hemolytic-uremic syndrome
*Nephrotic syndrome
Hepatic
Benign recuurent intrahepatic cholestasis
*Congenital biliary atresia
Acute and transient
Burns
Hepatitis
Others
Anorexia nervosa
Idiopathic hypercalcemia
Klinefelter syndrome
Progeria
Systemic lupus erythematosus
Werner syndrome
KwiterovichP:Disorders of lipid metabolism, in Rudolph AM (ed): Pediatrics, ed 17.
Hyperlipidemia in Childhood
Frederickson 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.
Hyperlipidemias
Fredrickson Classification
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
Hypercholesterolemia
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

Hypercholesterolemia
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
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 of the achilles and elbow
Tendon Xanthomas
tendon xanthomas of the hand
Cutaneous Xanthomas
Familial Hypercholesterolemia
Findings in Homozygotes
left coronary artery narrowing
supravalvar lipid deposition
Eye Findings in
Familial Hypercholesterolemia
Early corneal arcus
Cholesterol deposits in retinal fundus
Familial Hypercholesterolemia
Heterozygous 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

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 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
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.

Hypoalphalipoproteinemia

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
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

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 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 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
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

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 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 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 Screening
RISK ASSESSMENT
other concerning
risk factor
family history of
hypercholesterolemia
measure total
cholesterol
family history of
premature CAD
obtain lipoprotein
analysis
acceptable
(<170 mg/dl)
borderline
(170-199 mg/dl)
high
(>200 mg/dl)
repeat in 5 years
nutrition education
repeat and average
obtain lipoprotein
analysis
acceptable (<170)
repeat in 5 years
nutrition education
>170
obtain lipoprotein
analysis
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

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
LDL level
(repeat and average)
acceptable
(<110 mg/dl)
education on eating
and CAD risk factors
repeat lipoprotein analysis within 5 years
high
(>130 mg/dl)
borderline
(110-129 mg/dl)
evaluate for secondary causes
screen all family members
intensive clinical intervention
CAD risk factor advise
"Step One" diet
repeat lipoprotein analysis in 1 year
initiate "Step One" diet
set goal LDL
(at least < 130 mg/dl; ideally < 110 mg/dl)
repeat lipoprotein analysis in 6 weeks
GOAL NOT ACHIEVED
intensify "Step One" diet
GOAL ACHIEVED
continue long term monitoring
repeat lipoprotein analysis in 3 months
GOAL NOT ACHIEVED
initiate "Step 2" diet
GOAL NOT ACHEIVED AFTER
6 MONTHS TO 1 YEAR
continue "Step 2" diet
consider drug therapy
GOAL ACHIEVED
continue long term monitoring
GOAL ACHIEVED
continue long term monitoring
long term monitoring =
recheck lipoprotein
analysis 2x / year
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 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 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 Therapy
National Cholesterol Education Program (NCEP): Expert Panel on Blood Cholesterol Levels in Children and Adolescents
Mg of Cholesterol in Foods
cholesterol ( 300 mg/day)
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
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 Therapy
Fats and oils
·
·
·
·
SATURATED FATTY ACIDS are BAD
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 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
• 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
Exercise
• 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

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 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 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 Therapy
Bile-acid binding resins
Ezetimibe
HMG-CoA reductase inhibitors
(“statins”)
Niacin (nicotinic acid)
Fibric acid derivatives
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 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 Sequestrants
•Overall safe because not absorbed and lack
systemic toxicity
•However, they can cause malabsorption of fatsoluble 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 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 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)








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
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
Statins

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
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 interrelated factors such as genetics,
hypercholesterolemia, hypertension,
obesity, diabetes, and smoking
 Many of these risk factors are largely
preventable and/or modifiable

Hyperlipidemia in Childhood
Summary
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

Hyperlipidemia in Childhood