18
VOLUME 10 NUMBER 1 • MARCH 2013
REVIEW
SA JOURNAL OF DIABETES & VASCULAR DISEASE
Correspondence to: Prof Alan Sinclair
Institute of Diabetes for Older People, Bedfordshire
and Hertfordshire Postgraduate Medical School,
Putteridge Bury Campus, Hitchin Road, Luton LU2
8LE, Bedfordshire, UK.
Tel: +44(0) 1582 743285
E-mail:
Originally in:
Br J Diabetes Vasc Dis
2012;
12
: 65–70
S Afr J Diabetes Vascular Dis
2013;
10
: 18-22
Hypertriglyceridaemia in type 2 diabetes:
prevalence, risk and primary care management
ALAN SINCLAIR
Abstract
Cardiovascular disease (CVD) associatedwith type 2 diabetes
will impose an increasing burden on primary care over the
next few decades. Several mutually reinforcing factors
account for the increased CVD risk among patients with
diabetes, including hypertriglyceridaemia, the importance
of which has been generally underestimated. A consensus
from the literature suggests that fasting triglyceride levels
of 1.7 mmol/l or above may be a cause for cardiovascular
concern and warrant further investigation. Apart from CVD,
hypertriglyceridaemia can increase the risk of pancreatitis.
Clinicians in primary care should become active in identifying
and managing secondary causes of hypertriglyceridaemia
and encourage patients with diabetes to implement
lifestyle changes. Statins are the mainstay of treatment
for diabetic dyslipidaemia that remains inadequately
controlled. However, the National Institute for Health and
Clinical Excellence (NICE) suggests prescribing a fibrate if
triglyceride levels remain > 4.5 mmol/l after addressing
secondary causes. Clinicians could consider adding a fibrate
if triglyceride levels remain between 2.3 and 4.5 mmol/l
despite statin monotherapy for patients at high CVD risk.
NICE advocates a trial of highly concentrated, licensed
omega-3 fish oils if lifestyle measures and fibrate fail to
adequately reduce hypertriglyceridaemia.
Keywords:
cardiovascular disease, hypertriglyceridaemia,
type 2 diabetes mellitus, pancreatitis, primary care
Introduction
CVD in people with type 2 diabetes is likely to impose a growing
burden. The National Heart Forum predicts that rates of diabetes
will rise by 98% between 2006 (2 869 cases per 100 000 of the
population) and 2 050 (7 072 per 100 000).
1
Type 2 diabetes
accounts for 85–95% of cases of diabetes.
2
Patients with diabetes are at markedly higher risk of CVD,
3,4
partly because of an increased incidence of hypertriglyceridaemia,
5-7
a key component of diabetic dyslipidaemia that is also associated
with pancreatitis.
8,9
The paper attempts to stimulate primary care
physicians to manage lipid disorders in diabetes more proactively
and take evidence-based decisions when treating patients with
both diabetes and hypertriglyceridaemia.
Hypertriglyceridaemia and diabetes
Triglycerides evolved as an energy store and are found predominately
in adipose tissue. Chylomicrons and VLDLs transport most
triglycerides in the blood.
10
Chylomicrons are the main component
of postprandial lipoproteins,
11
while VLDL reflects hepatic synthesis.
5
In general, VLDL cholesterol begins rising substantially at triglyceride
concentrations of 2.26 mmol/l or higher.
5
Primary care physicians
can include triglycerides in a standard lipid profile request. While
treatment decisions should be based on fasted samples (which
reflects hepatic production), a non-fasted sample may offer some
indication of prevailing postprandial levels.
Hypertriglyceridaemia potentially results from increased
production of VLDL, reduced clearance of VLDL or chylomicrons,
or a combination of both mechanisms.
8
For example, insulin
modulates triglyceride levels, partly by inducing lipoprotein lipase,
which contributes to clearance of chylomicron triglycerides. The
rate of chylomicron clearance largely determines fasting and
postprandial triglyceride levels in patients with diabetes. However,
several other metabolic abnormalities appear to contribute to
diabetic hypertriglyceridaemia, including increased plasma VLDL
concentrations (with or without chylomicronaemia), increased
cholesterylester transfer protein activity and increased hepatic flux
of free fatty acids.
12
Moreover, many components of dyslipidaemia
Abbreviations and acronyms
AUC area under the curve
BMI
body mass index
CAD
coronary artery disease
CHD
coronary heart disease
CVD
cardiovascular disease
DHA
docosahexaenoic acid
EPA
eicosapentaenoic acid
FIELD
Fenofibrate Intervvention and Event Lowering in
Diabetes
HbA
1C
glycated haemoglobin A
1C
HDL
high-density lipoprotein
JELIS
Japan Eicosapentaenoic acid (EPA) Lipid Intervention
Study
LDL
low-density lipoprotein
MI
myocardial infarction
NICE
National Institute for Health and Clinical Excellence
PUFA
polyunstaturated fatty acid
RR
relative risk
VLDL
very low-density lipoprotein
