Objectives: Insulin-dependent diabetes mellitus (IDDM) is an autoimmune
disorder characterized by a variety of haemostatic abnormalities. The
purpose of this study was to investigate the levels of tetranectin (TN),
a regulator of fibrinolysis, in the plasma of IDDM children in relation
to HbA1c levels and to the state of platelet and endothelial cells
activation expressed by the levels of circulating P-selection
(cP-selectin) and VCAM-1 (cVCAM-1).
Patients and methods: TN, cP-selectin and cVCAM-1 levels were assessed
by ELISA in the plasma of 75 uncomplicated IDDM children and compared
with those of 33 healthy subjects. Patients were divided into subgroups
A and B according to the levels of HbA1c (HbA1c less than or equal to
6.8% and HbA1c > 6.8% respectively).
Results: TN levels have the tendency to be higher in IDDM children
[14.98(12.50-18.10) mg/L, P = 0.0210] compared to those in healthy
subjects [13.44(10.48-16.32) mg/L] and were significantly higher in
subgroup B than in subgroup A [16.92(13.48-18.26) mg/L vs
13.68(11.35-14.89) mg/L respectively, P = 0.0120]. The plasma levels of
cP-selectin and cVCAM-1 were significantly elevated in IDDM
[301(218-401) ng/ml, P = 0.0004 and 997(814-1222) ng/ml, P = 0.0015
respectively] than in healthy subjects [201(135-243) ng/ml, and
724(602-864) ng/ml respectively]. A trend towards higher cP-selectin
levels was observed in subgroup B compared to subgroup A. As regards
cVCAM-1, no statistically significant difference was found between
subgroups A and B. A significant correlation was found between
cP-selectin and cVCAM-1 (r(s) = 0.32, P = 0.034), while no correlation
was found between these variables and TN or HbA1c. However, a
significant correlation was observed between TN and HbA1c (r(s), = 0.37,
P = 0.011) in all IDDM patients. Likewise, a longitudinal follow up of
10 IDDM patients revealed a positive correlation between TN and HbA1c in
each patient.
Conclusions: These data provide evidence for VN elevation with the
increase of HbA1c in uncomplicated IDDM children, suggestive of TN
involvement in the haemostatic abnormalities in IDDM. The mechanism by
which this would occur is discussed
