Autoantibodies against autonomic nervous tissues in type 2 diabetes mellitus: no association with cardiac autonomic dysfunction.
There is evidence that autoimmune factors contribute to the pathogenesis of cardiac autonomic dysfunction in Type 1 Diabetes mellitus (DM). To evaluate the presence of autoantibodies against autonomic nervous tissues in Type 2 DM, 127 patients were studied for complement-fixing sympathetic and parasympathetic ganglia (CF-SG and CF-PSG) autoantibodies with an indirect immunofluorescence technique. Five cardiac reflex tests were performed to investigate cardiac autonomic neuropathy. QTc interval was assessed in all patients. As a control group, 60 healthy non-diabetic subjects were also tested for CF-SG and CF-PSG autoantibodies. CF-SG autoantibodies were detected in 11 (9%) and CF-PSG autoantibodies were observed in 7 (6%) Type 2 DM patients, whereas in control subjects, the frequency was 1 (2%) and 0 (0%) respectively (ns vs. Type 2 DM patients). In Type 2 DM patients with cardiac autonomic neuropathy (n=31, 24%), CF-SG autoantibodies and CF-PSG autoantibodies were detected in 3 (10%) patients, respectively, compared to 8 (8%) and 4 (4%) in Type 2 DM patients without cardiac autonomic neuropathy (n=96, 76%, ns v. Type 2 DM with cardiac autonomic neuropathy). Both CF-SG autoantibodies and CF-PSG autoantibodies were observed in 2 (7%) Type 2 DM patients with cardiac autonomic neuropathy and 3 (3%) Type 2 DM patients without cardiac autonomic neuropathy. Type 2 DM patients with cardiac autonomic neuropathy demonstrated a longer QTc-interval (446+/-42 ms) than Type 2 DM patients without cardiac autonomic neuropathy (413+/-45 ms, p=0.0001). In Type 2 DM patients with a prolonged QTc-interval (>440 ms: n=29, 23%), 2 (7%) patients presented with CF-SG and 3 (10%) had CF-PSG autoantibodies. In Type 2 DM, CF-SG and CF-PSG autoantibodies are not frequently observed. The results do not give evidence, that immunological factors--like in Type 1 DM--play a role in the pathogenesis of cardiac autonomic dysfunction in Type 2 DM.
Diabetes Research Institute, Munich, Germany. Oliver.Schnell@lrx.uni-muenchen.de
O
O
Schnell
A
A
Schwarz
D
D
Muhr-Becker
E
E
Standl
D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D003168:Complement Fixation Tests; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000097:blood / Q000276:immunology*; D004562:Electrocardiography; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005726:Ganglia, Parasympathetic / Q000276:immunology*; D005728:Ganglia, Sympathetic / Q000276:immunology*; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D007527:Isoenzymes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012016:Reference Values
D001323:Autoantibodies; D007527:Isoenzymes; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2