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Robert D. Hoeldtke, Kimberly D. Bryner, Gerald R. Hobbs, Gabriella G. Horvath, Jack E. Riggs, Ian Christie, Gary Ganser, Santica M. Marcovina, Ake Lernmark, Antibodies to Glutamic Acid Decarboxylase and Peripheral Nerve Function in Type 1 Diabetes, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 9, 1 September 2000, Pages 3297–3308, https://doi.org/10.1210/jcem.85.9.6830
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Abstract
Autoimmune mechanisms have been implicated in the pathophysiology of diabetic neuropathy. We studied the association between glutamic acid decarboxylase (GAD65) and islet cell (IA-2) autoantibodies as well as autoantibodies to the autonomic nervous system and peripheral nerve function in recent onset type 1 diabetes. Thirty-seven patients (27 females and 10 males) enrolled 2–22 months after diagnosis. Humoral factors, glycemic control, and peripheral nerve function were measured annually for 3 yr.
Patients with high GAD65Ab had worse glycemic control and higher insulin requirements. Patients with high GAD65Ab had slower motor nerve conduction velocities in the median, ulnar, and peroneal nerves (P < 0.025 for each nerve). The mean motor nerve conduction velocity Z scores at the time of the third evaluation was 0.341 ± 0.25 for the low GAD65Ab patients and −0.600 ± 0.25 for the high GAD65Ab patients (P < 0.01). Similar differences between the low and high GAD65Ab groups were observed for F wave latencies, thermal threshold detection, and cardiovascular autonomic function. The composite peripheral nerve function Z scores in the low GAD65Ab patients were 0.62 ± 11, 0.71 ± 0.19, and 0.21 ± 0.14 at the first, second, and third evaluations, significantly different from those in the high GAD65Ab patients in whom they were −0.35 ± 0.15, −0.46 ± 0.18, and −0.42 ± 0.16 (P < 0.001).
In summary, GAD65Ab in patients with recent onset type 1 diabetes are associated with worse glycemic control and slightly worse peripheral nerve function. Although the latter remained within normal limits and none of the patients had clinical neuropathy, the GAD65Ab-related differences in composite peripheral nerve function were highly significant (P < 0.001) and could not be attributed to GAD65Ab-related differences in glycemic control.
