To verify whether autoimmune markers related to nervous system structures a
nd other autoimmunity indexes present in diabetes mellitus are associated w
ith subclinical neuropathy, we examined 48 non-insulin-dependent diabetic p
atients with and without neuroelectrophysiological alterations. Nerve condu
ction velocity at the external sciatic-popliteal nerve, at the sural nerve,
at the median and ulnar nerves level has been evaluated. Autoimmunity was
investigated by evaluating glutamic acid decarboxylase (GAD-Ab), insulin (I
AA), GM3, GD3 and GT1b gangliosides, pancreatic islet cell (ICA) and anti-n
ervous-tissue autoantibody presence. Nerve conduction velocities were decre
ased in 72.9% of diabetic patients. Anti-insulin antibodies were detected i
n seven non-insulin treated diabetic patients and in higher amount in subje
cts with (17.1%) than in those without (7.7%) asymptomatic neuropathy. Anti
-GM3 antibodies were detected in four diabetic patients all of whom present
ed neurological complication. A significant correlation has been found betw
een neurological damage and presence of anti-insulin antibodies (p < 0.05).
In the case of GM3 autoantibody, a similar result was obtained, but the da
ta failed to reach statistical significance. Our data demonstrate that auto
immunity might play a role in the development of peripheral neuropathy, (C)
American Society for Histocompatibility and Immunogenetics, 1999. Publishe
d by Elsevier Science Inc.