O. Schnell et al., AUTOANTIBODIES AGAINST SYMPATHETIC-GANGLIA AND EVIDENCE OF CARDIAC SYMPATHETIC DYSINNERVATION IN NEWLY-DIAGNOSED AND LONG-TERM IDDM PATIENTS, Diabetologia, 39(8), 1996, pp. 970-975
Citations number
25
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
To investigate the presence of autoantibodies against sympathetic nerv
ous tissue and their correlation with cardiac sympathetic dysinnervati
on in insulin-dependent diabetes mellitus (IDDM), 20 newly diagnosed (
age 26 +/- 6 years) and 48 long-term IDDM patients (age 40 +/- 13 year
s, duration of diabetes 22 +/- 12 years) without myocardial perfusion
abnormalities (normal (TC)-T-99m-methoxyisobutylisonitrile uptake) wer
e assessed for myocardial I-123-metaiodobenzylguanidine (I-123-MIBG) u
ptake 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 subjec
ts (age 18-49 years) were investigated for CF-SG autoantibodies. Eight
newly diagnosed (40%) and 12 longterm (25%) IDDM patients exhibited C
F-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 I-123-MIBG up take correlated with CF-SG autoa
ntibodies (r = 0.34, p = 0.02). Newly diagnosed diabetic patients did
not show an association between CF-SG autoantibodies and global or reg
ional myocardial I-123-MIBG uptake. ECG-based cardiac autonomic neurop
athy (greater than or equal to two of five cardiac reflex tests abnorm
al) was present in 22 and absent in 26 long-term IDDM patients, of who
m 9 (41%) and 3 (12%), respectively were positive for CF-SG autoantibo
dies (p = 0.02). Only 1 newly diagnosed IDDM patient demonstrated ECG-
based cardiac autonomic neuropathy and was also positive for CF-SG aut
oantibodies. Although they are somewhat suggestive, results concerning
autoantibodies against sympathetic nervous tissue and cardiac sympath
etic dysinnervation do not strongly support the view that autoimmune m
echanisms play a major role in the pathogenesis of cardiac sympathetic
neuropathy in IDDM.