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Antibodies to glutamic acid decarboxylase and peripheral nerve function in type 1 diabetes

Hoeldtke, Robert D.; Bryner, Kimberly D.; Hobbs, Gerald R.; Horvath, Gabriella G.; Riggs, Jack E.; Christie, Ian; Ganser, Gary; Marcovina, Santica M. and Lernmark, Ake LU (2000) In Journal of Clinical Endocrinology and Metabolism 85(9). p.3297-3308
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... (More)

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.

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author
publishing date
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Contribution to journal
publication status
published
in
Journal of Clinical Endocrinology and Metabolism
volume
85
issue
9
pages
12 pages
publisher
The Endocrine Society
external identifiers
  • scopus:0033709495
ISSN
0021-972X
language
English
LU publication?
no
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5e96c852-0cd2-415a-b7e5-82cf65201cc4
date added to LUP
2017-09-06 14:52:11
date last changed
2017-09-06 16:42:56
@article{5e96c852-0cd2-415a-b7e5-82cf65201cc4,
  abstract     = {<p>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 &lt; 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 &lt; 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 &lt; 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 &lt; 0.001) and could not be attributed to GAD65Ab-related differences in glycemic control.</p>},
  author       = {Hoeldtke, Robert D. and Bryner, Kimberly D. and Hobbs, Gerald R. and Horvath, Gabriella G. and Riggs, Jack E. and Christie, Ian and Ganser, Gary and Marcovina, Santica M. and Lernmark, Ake},
  issn         = {0021-972X},
  language     = {eng},
  number       = {9},
  pages        = {3297--3308},
  publisher    = {The Endocrine Society},
  series       = {Journal of Clinical Endocrinology and Metabolism},
  title        = {Antibodies to glutamic acid decarboxylase and peripheral nerve function in type 1 diabetes},
  volume       = {85},
  year         = {2000},
}