Serum
Cholesterol levels do not change acutely with diet, whereas triglycerides do.
A random level may therefore be appropriate in many instances, but if a full profile is required, including HDL and LDL, a 12+ hour fasting blood sample should be collected
mmol/L
When classifying a lipid disorder for the purposes of treatment, three questions need to be asked:
– cholesterol only
– cholesterol and triglyceride
– triglyceride only
Secondary disorders
These are easily identified and when treated may entirely correct the lipid abnormalities.
The common causes are:
Primary disorders
If no secondary causes are identified the disorder is presumed to be primary.
There is a range of familial disorders which are presumptively identified by the family history or by physical signs such as xanthomata, corneal arcus.
The commonest familial disorders are familial hypercholesterolaemia and familial combined hyperlipidaemia. There are many others.
However, the commonest primary dyslipidaemia by a wide margin is polygenic hypercholesterolaemia, which is not familial. It is identified mainly by exclusion.
No significant family history, no abnormal physical signs.
Presumed to result from a combination of genetic and environmental factors, it provides a convenient diagnostic refuge.
Which lipid fractions are elevated?
Defining the abnormal fractions is important in both diagnosis and treatment.
The feature of familial hypercholesterolaemia is very high serum cholesterol.
The familial elevation of familial combined hyperlipidaemia may be cholesterol only (1/3), triglyceride only (1/3), or both (1/3).
Causes of secondary dyslipidaemias do not reliably produce a constant picture.
For example, though hypothyroidism typically causes elevation of cholesterol only, it can at times raise the triglyceride also.
Treatment
Dietary modification is common to the treatment of all dyslipidaemias.
Drug treatment, if required, will depend on whether the abnormality is cholesterol only (statins being the agent of choice), triglyceride only (fibrates usually first choice) or both.
A “fasting lipid screen” consists of:
1 day
Local test
Can be added on to an existing request up to 4 days following sample receipt
Individual lipids or lipid profile 30 days
Specimen Labelling Procedure
8210
