Lp(a) has atherogenic and thrombotic properties and is considered to b
e a major risk factor for the development of atherosclerotic disease.
The risk of cardiovascular disease is increased in both insulin-depend
ent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), and Lp
(a) has attracted attention as a potential risk factor in diabetic pat
ients. Lp(a) levels are ''probably'' elevated in IDDM patients and rel
ated to altered metabolic control and increased urinary albumin excret
ion rate or renal insufficiency, although results are controversial. T
here appears to be a real difference between the Lp(a) of patients wit
h proliferative diabetic retinopathy and those with or without backgro
und retinopathy. The plasma Lp(a) level may therefore be associated wi
th microangiopathy in some IDDM patients. However, data relating Lp(a)
to complications of diabetes are limited, a nd the literature is conf
licting. The few available data suggest that Lp(a) is not elevated in
NIDDM patients and that there is no strong link between blood glucose
control and plasma Lp(a). There is no clear evidence asto whether Lp(a
) is related to microalbuminuria in NIDDM patients. There is little ev
idence for a correlation between increased risk of cardiovascular dise
ase and plasma Lp(a) among diabetic patients. However, some diabetic p
atients with coronary heart disease have elevated plasma Lp(a), which
seems to be correlated with genetic factors (especially the isoforms o
f apolipoprotein a) rather than to diabetes per se. Lp(a) synthesis an
d catabolism could be influenced by insulin or by diabetes and its met
abolic concomitants. The atherogenic and thrombogenic potential of Lp(
a) could also be increased in diabetic patients. Plasma Lp(a) should b
e measured for both IDDM and NIDDM patients. If the Lp(a) level is ele
vated, it seems reasonable to check the other major vascular risk fact
ors.