M. Maioli et al., PLASMA APOLIPOPROTEIN(A) CONCENTRATION AND ISOFORMS IN SEVERE DIABETIC-RETINOPATHY, Diabetes, nutrition & metabolism, 8(4), 1995, pp. 219-225
mie previously showed that patients with long-standing insulin-depende
nt diabetes mellitus (IDDM) and severe diabetic retinopathy, resulting
from widespread capillary occlusion, have higher circulating levels o
f Lipoprotein(a) [Lp(a)] than IDDM patients without retinopathy or non
-diabetic controls. This study was aimed at: 1) confirming and extendi
ng that preliminary observation and 2) establishing whether heterogene
ous frequency of phenotypes distribution contributes to increase apoli
poprotein(a) [Apo(a)] concentrations in these patients. We studied 114
patients with IDDM of more than 15 years duration, of which 56 had se
vere retinopathy (proliferative and/or ischemic maculopathy) (SR) and
58 had no retinopathy(NR) and 60 non-diabetic control subjects(C). Hig
her Apo(a) levels were confirmed in patients with retinopathy but no d
ifference for the frequency of smaller Apo(a) isoforms was evident amo
ng the groups studied. However, among individuals with small isoforms,
SR patients had higher plasma Apo(a) concentrations than NR patients
and C group (p<0.05 for both). There was no relationship between the a
pparent molecular weight of Apo(a) isoforms and plasma Apo(a) concentr
ations within the three groups. These results suggest that Apo(a) poli
morphism is not an important genetic risk factor for severe diabetic r
etinopathy. If increased plasma Lp(a) plays a role in the pathogenesis
of this complication, non-genetic factors are likely to contribute.