title: Autoantibodies to sympathetic ganglia, GAD, or tyrosine phosphatase in long-term IDDM with and without ECG-based cardiac autonomic neuropathy.
abstract: OBJECTIVE
  To evaluate the association of autoantibodies to complement-fixing sympathetic ganglia (CF-SG), and tyrosine phosphatase (IA-2) with electrocardiogram (ECG)-based cardiac autonomic neuropathy (CAN) in long-term IDDM.
  
  
  METHODS
  We examined the prevalence of autoantibodies to CF-SG (by complement-fixing indirect immunoflourescence), GAD, and IA-2 (by radioligand assay) and islet cells (by indirect immunofluorescence) in 96 long-term IDDM patients (41 with ECG-based CAN, > or = 2 of 5 cardiac reflex tests abnormal; 55 without ECG-based CAN). As a control group, 89 healthy nondiabetic subjects were investigated.
  
  
  RESULTS
  CF-SG autoantibodies were observed more frequently in long-term IDDM patients than in the control group (25 vs. 4%, P = 0.0001). Of the IDDM patients, 14 (34%) with CAN and 10 (18%) without CAN presented with CF-SG autoantibodies (P = 0.06). GAD or IA-2 autoantibodies were detected in 14 (34%) and 17 (41%) IDDM patients with CAN, compared with 24 (44%) and 29 (53%) IDDM patients without CAN (P = 0.2, P = 0.2). Islet cell antibodies were observed in 6 (15%) IDDM patients with and in 9 (16%) IDDM patients without CAN (P = 0.5).
  
  
  CONCLUSIONS
  In long-term IDDM, the role of CF-SG autoantibodies, which tend to be more frequent in patients with ECG-based CAN, requires further investigations. The persistence of GAD and IA-2 autoantibodies is not related to ECG-based CAN.
authors.affiliation: Diabetes Research Institute, Schwabing City Hospital, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Muhr
authors.forename: U
authors.initials: U
authors.lastname: Mollenhauer
authors.forename: A G
authors.initials: AG
authors.lastname: Ziegler
authors.forename: M
authors.initials: M
authors.lastname: Haslbeck
authors.forename: E
authors.initials: E
authors.lastname: Standl
authors.forename: O
authors.initials: O
authors.lastname: Schnell
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000276:immunology* / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005728:Ganglia, Sympathetic / Q000276:immunology*; D005968:Glutamate Decarboxylase / Q000276:immunology; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000276:immunology; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000276:immunology; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D012016:Reference Values; D014636:Valsalva Maneuver
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D008565:Membrane Proteins; C516862:PTPRN protein, human; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase