Hypertriglyceridaemia is probably an independent risk factor for cardiac disease, but so far it hasn’t been possible to establish this for certain. (Interestingly, any relationship may be in a U-shaped curve, though it’s not at all clear where the peak would be – the PROCAM study showed 9 mmol/l but the Copenhagen Male Study showed 2.5 mmol/l.)
It also isn’t clear what the target should be. Official levels according to somebody-or-other’s guidelines are:
1.7 – 2.2 – borderline
2.3 – 5.5 – high
5.6 – 11 – very high
>11 – severe.
There are various forms of genetic primary hypertriglyceridaemias. The most common secondary causes are alcohol and obesity. Other causes include metabolic syndrome, DM, HIV (both the infection itself and its treatment), and the lipodystrophies, a collection of rare syndromes that may be congenital or acquired.
Triglycerides are the reason why we require 12-hour fasts before lipid profiles. Healthy people will actually need less than twelve hours, but the twelve hours allows for patients with metabolic abnormalities or established cardiovascular disease, who may take 12 hours (or more) for plasma concentrations to stabilise.
Recommended lifestyle changes are aimed partly at reducing the triglyceride levels and partly at reducing overall cardiovascular risk, and include:
- Weight reduction
- Smoking cessation
- Reduce alcohol intake, or abstain altogether if triglycerides very high
- Moderate carbohydrate intake (simple carbohydrates can worsen lipid profiles)
More detailed management is as follows:
Borderline: Goal: achieve LDL cholesterol targets. Management: lifestyle.
High: Primary goal: as for borderline. Secondary goal: achieve non-HDL targets. Management: lifestyle plus lipid-lowering therapy to achieve targets plus management of hyperglycaemia.
Very high: Primary goal: prevent pancreatitis. Secondary goal: prevent CVD. Management: Lifestyle changes including very low fat diet with fat forming <15% calorie intake. Triglyceride-lowering drug therapy including fish oil (4g/day long chain n-3 fatty acids).
Combined dyslipidaemia: statin +/- fibrate, or nicotinic acid.
Hypertriglyceridaemia: fibrate + omega-3 fatty acids.
Hypoalphalipoproteinaemia, whatever the heck that is: fibrate or nicotinic acid or omega-3 fatty acids.
(Ferns et al. Investigation and management of hypertriglyceridaemia. J Clin Pathol 2008; 61: 1174 – 83.)