Autoantibodies against sympathetic ganglia and evidence of cardiac sympathetic dysinnervation in newly diagnosed and long-term IDDM patients.
To investigate the presence of autoantibodies against sympathetic nervous tissue and their correlation with cardiac sympathetic dysinnervation in insulin-dependent diabetes mellitus (IDDM), 20 newly diagnosed (age 26 +/- 6 years) and 48 long-term IDDM patients (age 40 +/- 13 years, duration of diabetes 22 +/- 12 years) without myocardial perfusion abnormalities (normal 99mTC-methoxyisobutylisonitrile uptake) were assessed for myocardial 123I-metaiodo benzylguanidine (123I-MIBG) uptake and complement-fixing sympathetic ganglia (CF-SG) autoantibodies. Both groups of patients were also studied for islet cell antibodies (ICA) and ECG-based cardiac autonomic neuropathy. Eighty control subjects (age 18-49 years) were investigated for CF-SG autoantibodies. Eight newly diagnosed (40%) and 12 long-term (25%) IDDM patients exhibited CF-SG autoantibodies, compared to 4 control subjects (5%; p < 0.01, p < 0.05). In long-term diabetic patients, the reduction of global but not of regional myocardial 123I-MIBG uptake correlated with CF-SG autoantibodies (r = 0.34, p = 0.02). Newly diagnosed diabetic patients did not show an association between CF-SG autoantibodies and global or regional myocardial 123I-MIBG uptake. ECG-based cardiac autonomic neuropathy (> or = two of five cardiac reflex tests abnormal) was present in 22 and absent in 26 long-term IDDM patients, of whom 9 (41%) and 3 (12%), respectively were positive for CF-SG autoantibodies (p = 0.02). Only 1 newly diagnosed IDDM patient demonstrated ECG-based cardiac autonomic neuropathy and was also positive for CF-SG autoantibodies. Although they are somewhat suggestive, results concerning autoantibodies against sympathetic nervous tissue and cardiac sympathetic dysinnervation do not strongly support the view that autoimmune mechanisms play a major role in the pathogenesis of cardiac sympathetic neuropathy in IDDM.
Schsnell
O
O
Diabetes Research Institute, Munich, Germany.
Muhr
D
D
Dresel
S
S
Tatsch
K
K
Ziegler
A G
AG
Haslbeck
M
M
Standl
E
E
D019797:3-Iodobenzylguanidine; D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000096:biosynthesis*; D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000276:immunology*; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology* / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000209:etiology / Q000276:immunology*; D004562:Electrocardiography; D005260:Female; D005728:Ganglia, Sympathetic / Q000033:anatomy & histology / Q000276:immunology*; D006321:Heart / Q000294:innervation; D006331:Heart Diseases / Q000209:etiology / Q000276:immunology*; D006801:Humans; D007457:Iodine Radioisotopes; D007462:Iodobenzenes / Q000032:analysis / Q000378:metabolism; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D013565:Sympatholytics / Q000032:analysis / Q000378:metabolism; D015899:Tomography, Emission-Computed, Single-Photon
D001323:Autoantibodies; D007457:Iodine Radioisotopes; D007462:Iodobenzenes; D013565:Sympatholytics; D019797:3-Iodobenzylguanidine