July 23, 2017
Hyperlipidaemia Minimize



 Hyperlipidaemia is defined as an increase in the concentrations of cholesterol, triglycerides or both. "Normal values"  traditionally defined as 95% population ranges are not appropriate nowadays since the majority of western, and increasingly in developing, populations suffer from ischaemic heart disease. Reference values are therefore defined by decision points for treating patients with ischaemic heart disease. Patients with hypercholesterolaemia need to be investigated to determine whether they need treatment to prevent IHD and/or their families need to be studied.   Patients with hypertriglyceridaemia are most likely to have a secondary cause. However, it is important to recognise the primary cases since there is an increased risk of acute pancreatitis in individuals with very high concentrations of triglycerides.


One of the most difficult aspects of the diagnosis of hyperlipidaemia is the lack of conclusive diagnostic tests for most of the disorders. This is particularly important for the different forms of isolated hypercholesterolaemia, and to distinguish familial combined hyperlipidaemia from other causes of mild hypertriglyceridaemia (ie approx 2.5 -6 mmol/L).

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Effect of acute illness of lipids

An acute event eg myocardial infarction, has a profound effect on circulating lipids with a 30% fall in total cholesterol and 50% rise in triglycerides. These effects are maximal at 7 days and take approximately 3 months to resolve.

When are HDL-cholesterol and LDL-cholesterol subfractions useful?

The importance of lipoprotein analysis is in the evaluation of risk for individuals assessed for primary prevention of IHD. Patients with proven IHD should be given lipid lowering therapy with an aim of maintaining total cholesterol <  4.8 mmol/L (or LDL-cholesterol < 3.2 mmol/L). All patients starting lipid lowering therapy should have a full lipid profile to ensure that the total cholesterol is due to LDL-cholesterol and not HDL-cholesterol or triglyceride-rich particles. Raised HDL-cholesterol is particularly relevant for women who may retain a high HDL-cholesterol for many years after the menopause.


Lipoprotein (a) is pro-atherogenic lipoprotein with a structure similar to plasminogen and which binds to LDL-cholesterol. It is associated with an increased risk of IHD. However, it is nor routinely available since i) there are currently no therapies that reduce Lp(a) and ii) it is unstable in plasma and therefore not suitable for routine measurement.

Primary hypertriglyceridaemia

These are relatively rare and need to be diagnosed biochemically since eruptive xanthomata can occur with hypertriglyceridaemia of any cause. The differential diagnosis is i) remnant removal disease (usually but not always associated with the apo-E genotype E2:2), ii) lipoprotein lipase (or its' co-factor CII) deficiency or iii) familial hypertriglyceridaemia. The diagnosis of lipoprotein lipase deficiency is made on the failure of plasma lipase to rise after administration of IV heparin (exact protocol should be requested from the specialist laboratory performing this test); patients should have fasted overnight, refrained from alcohol for 24 hours and heavy exercise for 48 hours. Familial hypertriglyceridaemia is based on family studies and exclusion of the above disorders.

Random or fasting samples ?

The diagnosis of lipid abnormalities requires analysis of samples taken after 12 to 14 hour fast. However, since triglycerides rise by 200-300% after a meal, it is often useful to use random samples for screening since any abnormality in triglyceride pathways will be stressed and become apparent. There are minimal acute changes in total cholesterol and HDL-cholesterol in relation to meals and therefore for cardiac risk assessment, there is no need to take faasting blood samples.


  • JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice. Prepared by: British Cardiac Society, British Hypertension Society, Diabetes UK, HEART UK, Primary Care Cardiovascular Society, The Stroke Association Heart.2005; 91: v1-v52
  • Durrington PN. Dyslipidaemia. Lancet 2003;362:717-31.
  • The Emerging Risk FActors Collaboration. MAjor lipids, apolipoproteins, and risk of vascular disease. JAMA 2009;302:1993-2000.

JHB 11 Nov 2009


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