GLUTAMIC-ACID DECARBOXYLASE ANTIBODIES, AUTONOMIC NERVE ANTIBODIES AND AUTONOMIC NEUROPATHY IN DIABETIC-PATIENTS

To clarify whether GAD-ab are associated with diabetic autonomic neuro pathy and/or complement fixing antibodies against sympathetic ganglia, adrenal medulla, and vagus nerve, we examined 133 diabetic patients ( 95 with IDDM). GAD-ab were determined by a radioligand binding assay u sing in vitro expression of recombinant GAD-65 whereas sympathetic gan glia antibodies, adrenal medulla antibodies, vagus nerve, and ICA were evaluated by indirect immunofluorescence assays. Autonomic nerve func tion was evaluated by objective tests (heart rate reactions to deep br eathing and to tilt). In the total material of 133 patients, GAD-ab we re detected in 36 patients, all of whom had IDDM. The frequency of GAD -ab was similar (38 %) in IDDM patients with and without signs of auto nomic neuropathy (21 of 55 vs 15 of 40). In addition, there were no si gnificant associations between GAD-ab and autonomic nerve antibodies; GAD-ab were detected in 9 of 21 (43 %) of patients with and in 27 of 1 12 (24 %) of patients without sympathetic ganglia antibodies, in 5 of 15 (33 %) of patients with and 31 of 118 (26 %) without adrenal medull a antibodies, and in 5 of 15 (33 %) with and 31 of 118 (26 %) of patie nts without vagus nerve antibodies. The frequency of ICA, however, was significantly increased in patients with sympathetic ganglia antibodi es compared with those without sympathetic ganglia antibodies (10 of 2 1 [48 %] vs 21 of 112 [19 %];p < 0.01). In conclusion, GAD-ab were nei ther associated with disturbed autonomic nerve function nor with antib odies against autonomic nerve structures.