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Lipid profile
Short Description : Total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride
Also known as : [Cholesterol],[HDL],[LDL],[TRIG],[Triglycerides]


Plasma/Serum
Test performed by: LabPLUS Automation


Specimen Collection

The lipid profile includes the following tests: 

Both fast ing and non-fasting samples are acceptable

Sample stability:                           

Cholesterol         

  • 7 days at 15-25 o C             
  • 7days at 2-8 o C   
  • 3 months at -20 o C

HDL        

  • 72 hours at 15-25 o C                        
  • 7 days at 2-8 o C  
  • 12 months at -20 o C

Triglyceride         

  • 2 days at 20-25 o C                             
  • 10 days at 4 o C                   
  • 3 months at -20 o C


PST4.5 mL PST Blood (Preferred)
Micro-PST0.5 mL Paediatric Micro-PST Blood (Preferred)
Heparin5 mL Heparin Blood
Plain4 mL Plain Blood
SST3.5 mL SST Blood
Microsample0.5 mL Paediatric Microsample Blood
Micro-heparin0.5 mL Paediatric Micro-heparin Blood
Reference Intervals

For guidelines for interpretation and management of plasma lipids see the New Zealand Guideline Group website www.nzgg.org.nz.

All risk factors need to be taken into account when interpreting plasma lipid levels.

As a rough guide, the following levels are acceptable if no other major risk factors are present:

Adults

total cholesterol  <5.0
HDL cholesterol >1.0
LDL cholesterol <3.4
Triglyceride (TG) <2.0
total/HDL ratio <4.5
Non-HDL cholesterol <4.2

Non-HDL cholesterol is a measure of apoB containing particles (VLDL, VLDL remnants/IDL, LDL).   LDL are the smallest and risk/treatment guidelines have primarily focused on LDL, however the precursor VLDL and IDL particles are now also recognised as atherogenic.  These are usually present at low concentrations (0.8 mmol/L or less), but their concentration increases in clinical states of slow lipid particle clearance (e.g. diabetes, hypothyroidism, metabolic syndrome).  In such patients a raised non-HDL cholesterol can reflect increased concentrations of these triglyceride-rich particles, with increased CVD risk, even if LDL appears reassuring.  Such patients can also have a mildly-moderately raised triglyceride level.   In a non-fasting patient, a non-HDL cholesterol at or above 5.7 mmol/L (220mg/dL) also suggests a possible genetic dyslipidaemia.

Stone et al.  J Am Coll Cardiol. 2014;63(25_PA):2889-2934. doi:10.1016/j.jacc.2013.11.002

Patients <19 years old

Age Total cholesterol HDL cholesterol Triglyceride
0 - 14 days

1.2 - 3.2

0.4 - 1.1

0.9 - 3.0 

15 days - 1 year

1.6 - 6.2

0.3 - 1.9

0.6 - 3.0 

1 to 19 years 

2.9 - 5.4 

0.8 - 1.9

0.5 - 2.3 

Units : mmol/L

 

Uncertainty of Measurement:   

total cholesterol               4%

HDL-cholesterol              6%

Triglyceride                       5% 

 

Conversion factors

Cholesterol (total, HDL and LDL):  mg/100 mL x 0.026 = mmol/L
                                                               mmol/L x 38.6 = mg/100 mL

Triglyceride:  mg/100 mL x 0.0113 = mmol/L
                         mmol/L x 88.5 = mg/100 mL

Calculation of LDL- cholesterol is performed using the Friedwald formula:

LDL Cholesterol = Total Cholesterol - HDL Cholesterol - (TG x 0.456)

This calculation is only valid for fasting patients with serum triglyceride less than 4.5 mmol/L.

Calculation of Non-HDL cholesterol

Non-HDL cholesterol = Total cholesterol - HDL cholesterol

This is valid for non-fasting as well as fasting samples.



Turnaround Time: Within 3 hours
Diagnostic Use and Interpretation

Non-fasting Lipid Profiles

A non-fasting blood sample is acceptable for lipid tests in most cases. Screening for cardiovascular   risk assessment using the Framingham formula (and related risk algorithms) uses the total cholesterol / HDL ratio, which does not change after a meal.  

Triglyceride increases after food but the average increase is small (about 0.3 mmol/L). Triglyceride is not part of the Framingham risk algorithm; however evidence suggests non-fasting triglyceride levels are as good and possibly better at identifying patients with poor lipid particle clearance and who may be at increased CVD risk.   In Auckland there is consensus from experts that non-fasting lipids can be used to assess absolute risk, using algorithms such as PREDICT.

In most laboratories LDL is calculated from the other lipid levels, and this calculation is valid in non-fasting samples if the triglyceride is less than 4.5 mmol/L.   However, if the triglyceride is greater than 4.5 mmol/L, an LDL level cannot be calculated.  

The total of all atherogenic (apoB containing) particles can be expressed together as ?non-HDL cholesterol?.   This includes LDL as well as VLDL, IDL, and lipoprotein (a).   Non-HDL compares favourably with LDL as a CVD risk marker, especially in patients with poor lipid particle clearance where the proportion of non-LDL particles   is increased.   It does not require the patient to be fasting.   Non-HDL cholesterol can be easily calculated by the formula:  

Non-HDL cholesterol =   Total cholesterol   - HDL

 

Frequently asked questions:

What is the effect of a meal on lipid measurements?

There is little difference in most lipid parameters between fasting and non-fasting specimens after a typical meal (1-3).   Total cholesterol and LDL fall by about 0.2 mmol/L and HDL by about 0.1 mmol/L, for up to 3-4h. The TC/HDL ratio does not change.   These changes mostly reflect the dilution effect of water in the ingested food and are well within physiological variation of lipids typically seen in individual patients.  

Why has fasting previously been recommended for lipid and CVD risk assessment?

Most large population studies and intervention trials (e.g. statin trials) have used fasting samples.   However, there is no substantial evidence demonstrating fasting lipid levels to be superior to non-fasting levels for CVD risk prediction.   The parameter used in current Framingham-based risk algorithms (TC/HDL) can be used equally well.  

What evidence is there for the predictive value of non-fasting lipids on CVD risk?

Although evidence is less extensive than for fasting samples, a number of studies using non-fasting lipids (total cholesterol, HDL, TC/HDL ratio) have shown a strong association with CVD risk, and of similar magnitude to fasting results (about a 2-3 fold difference between subsets with highest and lowest TC/HDL) (4-6).  

How is LDL calculated, and are LDL measurements valid in non-fasting samples?

In most laboratories LDL is calculated from the other lipid levels, rather than being measured directly (7, 8).   Historically, the Friedewald equation has been used for many years:  LDL cholesterol = Total cholesterol - HDL cholesterol - Triglcyerides/2.2.  (All results in mmol/L)

The Friedewald equation crudely estimates the cholesterol fraction in triglyceride-rich particles (VLDL, chylomicrons), and has been used, despite it's problems, if the triglyceride result is less than 4.5 mmol/L.    However, as triglyceride levels rise, even below 4.5 mmol/L, the calculated LDL using this formula becomes progressively biased low , especially in patients on aggressive LDL-lowering treatment.  If the triglyceride is greater than 4.5 mmol/L, an LDL level cannot be calculated using the Friedewald formula and no result can be issued.  

From 21/09/2021 LabPlus and the Auckland laboratory Regional Quality Assurance Group has adopted a new formula, the Sampson formula, to calculate LDL. This equation is much better than the previous Friedewald equation at recognizing the non-linear contribution of cholesterol in triglyceride rich lipoproteins .

The Sampson calculation shows much less bias from triglyceride elevation, and is valid for triglycerides levels below 9.0 mmol/L. However, if the triglyceride is equal to or greater than 9.0 mmol/L, an LDL level still cannot be calculated. 

What about triglycerides?

In healthy people triglycerides rise about 15-20%, or about 0.2-0.3 mmol/L (2,4), after a meal (for up to 6-8h)(1).   Some patients have slow lipid particle clearance after food (so-called ?post-prandial dyslipidaemia?).   They typically have a high triglyceride and low HDL pattern even on fasting samples.   However, non-fasting triglycerides may even better predictive value for future CVD events in such patients (9,10).   Therefore an initial non-fasting sample is also reasonable.   The disadvantage is that accurate ranges are less well documented than for fasting measurements, but   non-fasting triglycerides above 2 mmol/L is suspicious for such ?postprandial dyslipidaemia? unless explained by some other factor, such as alcohol or oestrogens(11).

When, if ever, should fasting samples be taken?

The specific indications for a fasting are limited, especially as fasting glucose is also no longer considered the first line screening test for diabetes.   The clearest reason is in patients with high triglycerides being monitored with lifestyle or drug intervention, where a f asting sample is better standardised.   If fasting triglyceride levels fall below 4.5 mmol/L then calculated LDL can also be reported in such patients.

What is the value of non-HDL cholesterol?

Although the modern emphasis is not on strict cholesterol treatment targets, but rather a risk-based approach, historically non-HDL treatment targets were usually about 0.8 mmol/L   higher than LDL targets. In a non-fasting patient, a non?HDL level of 5.7 mmol/L or more may indicate genetic hypercholesterolemia that requires further evaluation or a secondary cause (13) .  

 

References:

1. Langsted A, Freiberg JJ and Nordesgaard BG.   Fasting and non-fasting lipid levels: influence of normal food intake on lipids, lipoproteins, apoproteins and cardiovascular risk prediction. Circulation 2008; 118: 2047-56.

2. Sidhu D, Naugler C. Fasting time and lipid levels in a community-based population: a cross-sectional study [published online November 12, 2012]. Arch Intern Med . 2012;172: 1707-1710.

3. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106: 3143?3421.

4. Mora S, Rifai N, Buring JE, and Ridker PM. Fasting compared with non-fasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation 2008; 118: 993-1001

5. Di Angelantonio E, Sarwar N, Perry P, et al.   Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA . 2009; 302:1993-2000.

6. Khera AV, Mora S. Fasting for lipid testing.   Is it worth the trouble?   Arch. Int. Med. 2012; 172: 1710-2

7. Friedewald WT, Levy RI, and Fredrickson DS.   Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without the use of the preparative ultracentrifuge. Clin Chem 1972;18: 499 ? 502.

8.   Mora S, Rifai N, Buring JE, Ridker PM. Comparison of LDL cholesterol concentrations by Friedewald calculation and direct measurement in relation to cardiovascular events in 27 331 women. Clin Chem 2009; 55: 888-94

9. Sampson M, Ling C, Sun Q et al., A New Equation for Calculation of Low-Density Lipoprotein Cholesterol in Patients With Normolipidemia and/or Hypertriglyceridemia. JAMA Cardiol. 2020 May 1;5(5):540-548.

10. Bansal S, Buring JE, Rifai N, et al. Fasting compared with non-fasting triglycerides and risk of cardiovascular events in women. JAMA 2007; 298: 309-16

11. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA . 2007;298:299 ?308.

12. Watts GF and Kohn JS. Whither the lipid profile? Feast, famine, or no free lunch?   Clin. Chem. 57:363-5

13. www.ifcc.org (keyword ?non-HDL cholesterol?)

14. Stone, NJ, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.    J. Am. Coll. Cardiol. 2014 Jul 1;63 (25 Pt B): 2889-934.

 


Contact Information

Emails to chemicalpathologist@adhb.govt.nz will receive priority attention from the on-call chemical pathologist.

If the query concerns a specific patient please include the NHI number in your email.

If email is not a suitable option, please contact the on-call chemical pathologist via Lablink (Auckland City Hospital ext. 22000 or 09-3078995).

Individual chemical pathologists may be contacted but will not be available at all times. 

After-hours : contact  Lablink (Auckland City Hospital ext. 22000 or 09-3078995) or hospital operator for on duty staff after hours.


Dr Cam Kyle (Clinical Head): CampbellK@adhb.govt.nz   ext 22052 

Dr Weldon Chiu: WeldonC@adhb.govt.nz   ext. 23427 

Dr Leah Ha: LHa@adhb.govt.nz  ext. 23427

Dr Samarina Musaad: SamarinaM@adhb.govt.nz ext. 22402 

Dr Leo Lam: ChiSingL@adhb.govt.nz  ext 22574



Last updated at 11:01:48 13/09/2021