(Adults)
LIPID PROFILE, EXTENDED ,
SERUM
(Spectrophotometry,
Electrophoresis
&Immunoturbidimetry)
-
Cholesterol, Total
Triglycerides
HDL Cholesterol
LDL Cholesterol
VLDL Cholesterol
Non HDL Cholesterol
Chylomicrons
-
Cholesterol: HDL Ratio
mg/dL
mg/dL
mg/dL
mg/dL
mg/dL
mg/dL
<200
<150
-
3.30-4.40
<100
<30
<130
Nil
Apolipoproteins B / A 1 Ratio
Apo A1
105-205 ( Females)
105-175 ( Males)
55-130 ( Females)
60-140 ( Males)
(0.35-0.98)
mg/dL
Apo B
mg/dL
Apo B / Apo A1 Ratio
Lipoprotein (a); Lp(a)
mg/dL
< 30
Cardio CRP
mg/L
<1.00
Lipoprotein electrophoresis
HDL
LDL
VLDL
Chylomicrons
%
%
%
-
15.10-39.90
42.30-69.50
2.00-31.20
Nil
HDL Cholesterol
>50
>40
Gender
Females
Males
Interpretation
NATIONAL LIPID
ASSOCIATION
RECOMMENDATIONS
(NLA-2014)
Optimal
TOTAL
CHOLESTEROL in
mg/dL
TRIGLYCERIDE
in mg/dL
LDL
CHOLESTEROL in
mg/dL
NON HDL
CHOLESTEROL
in mg/dL
<200
<150
<100
<130
Above Optimal
Borderline High
High
Very High
REMARKS
Low risk
Average risk
Moderate risk
High risk
200-239
>=240
-
CHOLESTEROL : HDL
RATIO
3.3-4.4
4.5-7.1
7.2-11.0
>11.0
REMARKS
Optimal
Above Optimal
Borderline High
High
Very High
REMARKS
Low risk
Average risk
Moderate
risk
High risk
Cholesterol : HDL
Ratio
3.3-4.4
4.5-7.1
7.2-11.0
>11.0
150-199
200-499
>=500
CARDIO CRP in
(mg/L)
<1.0
1.0-3.0
>3.0
TOTAL
CHOLESTEROL in
mg/dL
<200
200-239
>=240
-
100-129
130-159
160-189
>=190
130 - 159
160 - 189
190 - 219
>=220
APO B in (mg/dL)
Lp (a) in(mg/dL)
<80
80-119
>=120
>=50
TRIGLYCERIDE in
mg/dL
LDL CHOLESTEROL
in mg/dL
<150
150-199
200-499
>=500
<100
100-129
130-159
160-189
>=190
Apo B / A1 Ratio
0.35-0.98
>0.98
Note: 1. Measurements in the same patient can show physiological& analytical variations. Three
serial samples 1 week apart are recommended for Total Cholesterol, Triglycerides, HDL& LDL
Cholesterol
2. As per NLA-2014 guidelines, all adults above the age of 20 years should be screened for
lipid
status. Selective screening of children above the age of 2 years with a family history of
premature cardiovascular disease or those with at least one parent with high total
cholesterol is
recommended.
3. NLA-2014 identifies Non HDL Cholesterol(an indicator of all atherogenic lipoproteins such
as LDL , VLDL, IDL, Lpa, Chylomicron remnants)along with LDL-cholesterol as co- primary
target for cholesterol lowering therapy. Note that major risk factors can modify treatment
goals for LDL &Non HDL.
4.Apolipoprotein B is an optional, secondary lipid target for treatment once LDL & Non HDL
goals have been achieved
5. If initial cardio CRP>10mg/L, it should be disregarded & measured again when patient
stabilizes. Avoid measurement during acute infection, chronic inflammatory disease, post
menopausal hormone therapy
6. If initial cardio CRP<10mg/L – use average of two values (measured 2 or more weeks
apart;intraindividual variation being >40%) to estimate risk
Comments
The NCEP ATP III guidelines established LDL-C& Non LDL-C treatment goals in 2004 since then use of
lipid lowering drugs particularly statins has reduced Atherosclerotic Cardiovasular disease (ASCVD)
morbidity and mortality; however significant residual risk for the events remains. This combined
with the rising prevalence of obesity, which has shifted the risk profile of the population toward
patients in whom LDL -C is less predictive of ASCVD events (metabolic syndrome, low HDL
Choleterol, elevated triglycerides). NLA 2014, recommended for those at moderate risk (2 major
ASCVD risk), additional testing for inflammatory, non-lipid and other lipid biomarkers may be
considered for risk refinement. The presence of one or more secondary risk factor should prompt
the clinician to consider drug therapy for patient whose atherogenic cholesterol level is higher than
goal level
Major risk factors for ASCVD


Age ( men >=45; women >=55)
Family history of premature CHD (CHD in a male first degree relative < 55 years / CHD in a
female first degree relative < 65 years)



Cigarette smoking
Hypertension ( BP >= 140/90 or on antihypertensive medication)
Low HDL Cholesterol ( <40 mg/dL in males and <50 mg/dL in females)


Diabetes mellitus
Pre-existing ASCVD
Secondary risk indicators for risk refinement



Coronary artery calcium (>300 A considered high risk)
LDL-C >160mg/dl and/or Non HDL-C >190 mg/dL
hsCRP>2.0mg/L


Lp(a) > 50mg/dl
Urine Albumin/Creatinine ratio>30mg/gCrt
Cholesterol:There is a clear cut relationship between elevated serum cholesterol and
myocardial infarction. At the tissue level, it plays a prominent part in atherosclerotic lesions.
Triglycerides: Elevated levels are seen with overnight fast less than 12 hours, Non insulin
dependent Diabetes mellitus, Obesity, Alcohol intake, Hyperlipidemias (specially Types I, IV
& V; > 1000), Pancreatitis ( > 500), Gout, Pregnancy, Drugs like thiazide diuretics, anabolic
steroids, cholestyramine, corticosteroids, amiodarone& interferon.
HDL Cholesterol: It is a cardioprotective cholesterol ( good cholesterol). Patients with low
levels of HDL are at increased risk for premature ASCVD and is used in risk factor counting
and quantitative risk assessment.HDL cholesterol levels are inversely related to an increase
in body fat, waist circumference, triglyceride, small dense LDL particles, insulin resistance,
systemic inflammation & cigarette smoking.
LDL and Non HDL Cholesterol:LDL-C has traditionally been the primary target of therapy,
the NLA Expert Panel consensus view is that Non HDL-C is a better primary target for
modification than LDL-C. Non HDL-C comprises the cholesterol carried by all potentially
atherogenic particles, including LDL,IDL, VLDL, VLDL & Chylomicron remnants and Lp(a). Non
HDL-C also simplifies the management of patients with high triglycerides as it incorporates
triglyceride concentration indirectly.
Apolipoprotein B: Each potentially atherogenic lipoprotein particlecontains one molecule of Apo B
thus it is a direct indicator of number of circulating particles with atherogenic potential. Apo B is
more powerful independent predictor of ASCVD than LDL Cholesterol. Apo B is a potential
contributor to residual ASCVD risk because it may remain elevated in some individuals (especially
those with elevated triglyceride and lower HDL cholesterol) who have attained there treatment
goals for Non-HDL & LDL cholesterol. In NLA recommendation, 2014 Apo B is considered as an
optional, secondary target for treatment
Lipoprotein (a); Lp(a): Increased levels are usually familial showing an autosomal dominant
pattern of inheritance and are associated with an increased risk of ASCVD, Cerebrovascular
disease and Stroke. Generally the levels are not influenced by diet or common
hyperlipidemicdrugs but can be lowered by Niacin (Vitamin B3), Exercise, Neomycin &
Estrogen replacement therapy.
Cardio CRP: Elevated CRP levels is a risk factor for ASCVD that is independent of patient’s
LDL value. Cardio CRP is a strong indicator of future cardiovascular events. Patients with
elevated CRP levels may have greater benefit in risk reduction with statin therapy than
those with lower CRP levels independent of LDL cholesterol values.
Usage

Patients with two major risk factors for ASCVD

Patients with hypertriglyceridemia/metabolic syndrome/abdominal obesity/insulin
resistance
 Patients with normal lipid profile but low HDL
 Patients on Statin therapy who have achieved desirable LDL-C & non HDL-C goals
 Clinical evidence of non CHD atherosclerosis or DM
 Family h/o premature CHD especially patients with Familial combined Hyperlipidemia (Tg>
150 mg/dl & Apo B > 120 mg/dl) which is the most common cause of premature CHD
 Familial HYpercholeterolemia
Recurrent ASCVD events
Comment
A variety of genetic conditions are associated with accumulation in plasma of specific class
of lipoprotein particles. The critical first step in managing lipid disorder is to determine the
class or classes of lipoprotein that are increased or decreased in a patient. Frederickson
classification can be helpful in this regard. The hyperlipidemic status should be evaluated to
determine if it is a primary lipoprotein disorder or secondary to metabolic disease. The
diagnosis of primary hyperlipidemia is made after secondary causes have been ruled out. It
is important to diagnose primary lipid disorder since the underlying etiology has significant
effect on development of CHD, on response to drug therapy, and on the management of
other family members. Type II b is the most commonly inherited lipid disorder, occurring in
approximately 1 in 200 persons.Familial hypertriglyceridemia (FHTG) is a relatively common
(1:500) autosomal dominant disorder of unknown etiology. It is important to consider & rule
out secondary causes of hypertriglyceridemia (Obesity, Type 2 DM, Alcoholism, Renal failure,
Cushing's syndrome etc.) before making the diagnosis of FHTG.
FREDRICKSON CLASSIFICATION
Type of
Hyperlipoproteinemia
Molecular
defect
Estimated
incidence
Lipoprotein
elevated
I
Familial
Chylomicronemia
Syndrome
Lipoprotien
lipasedefici
ency; Apo C
II
deficiency
Mutation in
LDL
receptor,
Apo B 100
1 in
1,000,000
Chylomicro
ns
1 in 500
LDL
II a
Familial
Hypercholesterolemia
Cholester
ol, Total
(mg/dL)
+ to ++
200-400
Triglyceride
(mg/dL)
Serum
Appearance
++++
> 3000
Milky
+++
300-1000
Normal
Clear
II b
Familial Combined
Hyperlipidemia
Unknown
1 in 200
LDL & VLDL
++ to +++
280- 350
++
200-500
Clear to
slightly turbid
III
Familial
Dysbetalipoproteinemi
a or Familial
broadbetadisease
Genetic
variation in
APO E
1 in 10,000
Chylomicro
n and VLDL
remnant
(IDL)
++ to +++
300- 500
++ to +++
200- 900
Clear to
slightly turbid
IV
Familial
hypertriglyceridemia
Unknown
1 in 500
VLDL
Usually
<270
++
200-1000
Turbid
1 in 500
Chylomicro
n & VLDL
++ to +++
<500
++++
<3000
Milky
V
Familial
hypertriglyceridemia
Unknown
(Children)
LIPID PROFILE, EXTENDED ,
SERUM
(Spectrophotometry,
Electrophoresis
&Immunoturbidimetry)
-
Cholesterol, Total
Triglycerides
HDL Cholesterol
LDL Cholesterol
VLDL Cholesterol
Non HDL Cholesterol
Chylomicrons
Cholesterol: HDL Ratio
-
mg/dL
mg/dL
mg/dL
mg/dL
mg/dL
mg/dL
Nil
-
Apolipoproteins B / A 1 Ratio
Apo A1
mg/dL
Apo B
mg/dL
Apo B / Apo A1 Ratio
Lipoprotein (a); Lp(a)
<170
<150
40-60
<110
<30
mg/dL
3.30-4.40
105-205 ( Females)
105-175 ( Males)
55-130 ( Females)
60-140 ( Males)
(0.35-0.98)
< 30
Cardio CRP
mg/L
<1.0
Lipoprotein electrophoresis
HDL
LDL
VLDL
Chylomicrons
%
%
%
-
15.1-39.9
42.3-69.5
2.0-31.2
Nil
REMARKS
Optimal
Borderline High
High
Very High
REMARKS
Low risk
Average risk
Moderate risk
High risk
TOTAL
CHOLESTEROL in
mg/dL
<170
171-199
>=200
-
CHOLESTEROL : HDL RATIO
3.3-4.4
4.5-7.1
7.2-11.0
>11.0
REMARKS
Low risk
Average risk
Moderate
risk
High risk
Cholesterol : HDL
Ratio
3.3-4.4
4.5-7.1
7.2-11.0
>11.0
TRIGLYCERIDE in
mg/dL
LDL CHOLESTEROL
in mg/dL
<150
150-199
200-499
>=500
<110
111-129
>=130
-
CARDIO CRP in (mg/L)
<1.0
1.0-3.0
>3.0
APO B in (mg/dL)
<80
80-119
>=120
Lp (a) in(mg/dL)
>=50
Apo B / A1 Ratio
0.35-0.98
>0.98
Note: 1. Measurements in the same patient can show physiological& analytical variations. Three
serial samples 1 week apart are recommended for Total Cholesterol, Triglycerides, HDL& LDL
Cholesterol
2. . As per NLA-2014 guidelines, all adults above the age of 20 years should be screened for
lipid
status. Selective screening of children above the age of 2 years with a family history of
premature cardiovascular disease or those with at least one parent with high total
cholesterol is
recommended.
3. NLA-2014 identifies Non HDL Cholesterol(an indicator of all atherogenic lipoproteins such
as LDL , VLDL, IDL, Lpa, Chylomicron remnants)along with LDL-cholesterol as co- primary
target for cholesterol lowering therapy. Note that major risk factors can modify treatment
goals for LDL &Non HDL.
4.Apolipoprotein B is an optional, secondary lipid target for treatment once LDL & Non HDL
goals have been achieved
5. If initial cardio CRP>10mg/L, it should be disregarded & measured again when patient
stabilizes. Avoid measurement during acute infection, chronic inflammatory disease, post
menopausal hormone therapy
6. If initial cardio CRP<10mg/L – use average of two values (measured 2 or more weeks
apart;intraindividual variation being >40%) to estimate risk
Comments
The NCEP ATP III guidelines established LDL-C& Non LDL-C treatment goals in 2004 since then use of
lipid lowering drugs particularly statins has reduced Atherosclerotic Cardiovasular disease (ASCVD)
morbidity and mortality; however significant residual risk for the events remains. This combined
with the rising prevalence of obesity, which has shifted the risk profile of the population toward
patients in whom LDL -C is less predictive of ASCVD events (metabolic syndrome, low HDL
Choleterol, elevated triglycerides). NLA 2014, recommended for those at moderate risk (2 major
ASCVD risk), additional testing for inflammatory, non-lipid and other lipid biomarkers may be
considered for risk refinement. The presence of one or more secondary risk factor should prompt
the clinician to consider drug therapy for patient whose atherogenic cholesterol level is higher than
goal level
Major risk factors for ASCVD


Age ( men >=45; women >=55)
Family history of premature CHD (CHD in a male first degree relative < 55 years / CHD in a
female first degree relative < 65 years)



Cigarette smoking
Hypertension ( BP >= 140/90 or on antihypertensive medication)
Low HDL Cholesterol ( <40 mg/dL in males and <50 mg/dL in females)


Diabetes mellitus
Pre-existing ASCVD
Secondary risk indicators for risk refinement





Coronary artery calcium (>300 A considered high risk)
LDL-C >160mg/dl and/or Non HDL-C >190 mg/dL
hsCRP>2.0mg/L
Lp(a) > 50mg/dl
Urine Albumin/Creatinine ratio>30mg/gCrt
Cholesterol:There is a clear cut relationship between elevated serum cholesterol and
myocardial infarction. At the tissue level, it plays a prominent part in atherosclerotic lesions.
Triglycerides: Elevated levels are seen with overnight fast less than 12 hours, Non insulin
dependent Diabetes mellitus, Obesity, Alcohol intake, Hyperlipidemias (specially Types I, IV
& V; > 1000), Pancreatitis ( > 500), Gout, Pregnancy, Drugs like thiazide diuretics, anabolic
steroids, cholestyramine, corticosteroids, amiodarone& interferon.
HDL Cholesterol: It is a cardioprotective cholesterol ( good cholesterol). Patients with low
levels of HDL are at increased risk for premature ASCVD and is used in risk factor counting
and quantitative risk assessment.HDL cholesterol levels are inversely related to an increase
in body fat, waist circumference, triglyceride, small dense LDL particles, insulin resistance,
systemic inflammation & cigarette smoking.
LDL Cholesterol:LDL-C has traditionally been the primary target of therapy, the NLA Expert
Panel consensus view is that Non HDL-C is a better primary target for modification than LDLC. Non HDL-C comprises the cholesterol carried by all potentially atherogenic particles,
including LDL,IDL, VLDL, VLDL & Chylomicron remnants and Lp(a). Non HDL-C also simplifies
the management of patients with high triglycerides as it incorporates triglyceride
concentration indirectly.
Apolipoprotein B: Each potentially atherogenic lipoprotein particlecontains one molecule of Apo B
thus it is a direct indicator of number of circulating particles with atherogenic potential. Apo B is
more powerful independent predictor of ASCVD than LDL Cholesterol. Apo B is a potential
contributor to residual ASCVD risk because it may remain elevated in some individuals (especially
those with elevated triglyceride and lower HDL cholesterol) who have attained there treatment
goals for Non-HDL & LDL cholesterol. In NLA recommendation, 2014 Apo B is considered as an
optional, secondary target for treatment
Lipoprotein (a); Lp(a): Increased levels are usually familial showing an autosomal dominant
pattern of inheritance and are associated with an increased risk of ASCVD, Cerebrovascular
disease and Stroke. Generally the levels are not influenced by diet or common
hyperlipidemic drugs but can be lowered by Niacin (Vitamin B3), Exercise, Neomycin &
Estrogen replacement therapy.
Cardio CRP: Elevated CRP levels is a risk factor for ASCVD that is independent of patient’s
LDL value. Cardio CRP is a strong indicator of future cardiovascular events. Patients with
elevated CRP levels may have greater benefit in risk reduction with statin therapy than
those with lower CRP levels independent of LDL cholesterol values.
Usage

Patients with two major risk factors for ASCVD

Patients with hypertriglyceridemia/metabolic syndrome/abdominal obesity/insulin
resistance
 Patients with normal lipid profile but low HDL
 Patients on Statin therapy who have achieved desirable LDL-C & non HDL-C goals
 Clinical evidence of non CHD atherosclerosis or DM
 Family h/o premature CHD especially patients with Familial combined Hyperlipidemia (Tg>
150 mg/dl & Apo B > 120 mg/dl) which is the most common cause of premature CHD
 Familial HYpercholeterolemia
Recurrent ASCVD events
Comment
A variety of genetic conditions are associated with accumulation in plasma of specific class
of lipoprotein particles. The critical first step in managing lipid disorder is to determine the
class or classes of lipoprotein that are increased or decreased in a patient. Frederickson
classification can be helpful in this regard. The hyperlipidemic status should be evaluated to
determine if it is a primary lipoprotein disorder or secondary to metabolic disease. The
diagnosis of primary hyperlipidemia is made after secondary causes have been ruled out. It
is important to diagnose primary lipid disorder since the underlying etiology has significant
effect on development of CHD, on response to drug therapy, and on the management of
other family members. Type II b is the most commonly inherited lipid disorder, occurring in
approximately 1 in 200 persons.Familial hypertriglyceridemia (FHTG) is a relatively common
(1:500) autosomal dominant disorder of unknown etiology. It is important to consider & rule
out secondary causes of hypertriglyceridemia (Obesity, Type 2 DM, Alcoholism, Renal failure,
Cushing's syndrome etc.) before making the diagnosis of FHTG.
FREDRICKSON CLASSIFICATION
Type of
Hyperlipoproteinemia
Molecular
defect
Estimated
incidence
Lipoprotein
elevated
Cholester
ol, Total
(mg/dL)
Triglyceride
(mg/dL)
Serum
Appearance
I
Familial
Chylomicronemia
Syndrome
Lipoprotien
lipasedefici
ency; Apo C
II
deficiency
Mutation in
LDL
receptor,
Apo B 100
Unknown
1 in
1,000,000
Chylomicro
ns
+ to ++
200-400
1 in 500
LDL
+++
300-1000
1 in 200
LDL & VLDL
++ to +++
280- 350
++
200-500
Clear to
slightly turbid
III
Familial
Dysbetalipoproteinemi
a or Familial
broadbetadisease
Genetic
variation in
APO E
1 in 10,000
Chylomicro
n and VLDL
remnant
(IDL)
++ to +++
300- 500
++ to +++
200- 900
Clear to
slightly turbid
IV
Familial
hypertriglyceridemia
Unknown
1 in 500
VLDL
Usually
<270
++
200-1000
Turbid
1 in 500
Chylomicro
n & VLDL
++ to +++
<500
++++
<3000
Milky
II a
Familial
Hypercholesterolemia
II b
Familial Combined
Hyperlipidemia
V
Familial
hypertriglyceridemia
Unknown
++++
> 3000
Normal
Milky
Clear