engleski

Glutamic acid decarboxylase autoantibody is associated with peripheral neuropathy in autoimmune diabetes in adults

Mechanisms implicated into the pathogenesis of autoimmune diabetes (AI) may also play a role in the development of peripheral diabetic neuropathy (PDN). A possible link between glutamic acid decarboxylase autoantibody GAD Ab) and PDN in patients with type 1 diabetes was recently reported. We investigated the association between GAD Ab, islet cell antigen (ICA Ab) and insulinoma associated protein-2 (IA-2 Ab) with PDN in AI diabetes in adults. Four hundred and 61 patient (mean age 42y) positive for at least one diabetes related Ab at the time of diagnosis were included and divided according to the presence of PDN into two groups. ICA was measured by indirect immunofluorescence while GAD and IA2 were detected with ELISA. Peripheral neuropathy was determined by electroneurography. PDN was present in 76.1% patients. Patients with PDN were older (43 vs. 37 y, p=0.031), had longer disease duration (11 vs. 9 y, p=0.138), higher rate of hypertension (30.4 vs. 26.0, p=0.016) and statin use (18.8 vs. 15.3% p=0.046), better glycaemic control (7.2 vs. 7.5% p=0.029) but increased C reactive protein (5.7 vs. 4.9 mg/dL, p=0.6) and ferritin (296.6 vs. 195.9 µg/L, p=0.015) level. The Ab status in the group with PDN revealed significantly higher GAD Ab (430.9 vs. 96.65, p=0.001), lower ICA (27.5 vs. 150 JDF.p=0.001) and similar IA-2 titer (205.7 vs. 238.1 U/L. p=0.593). A significant correlation between GAD Ab titer and ferritin level was found (r=0.37, p=0.001). In the multinominal regression including age, gender, disease duration, A1c, ICA, GAD and IA- 2, GAD titer was independently associated with PDN (1.392 (1.113-1.198)). In AI diabetes in adults GAD Ab titer is associated with presence of PDN and the relation seems to be independent of age, disease duration or glycaemic control. The association between GAD Ab and serum ferritin as a marker of cell stress might indicate GAD Ab mediated systemic inflammatory process implicated in the pathogenesis of PDN that merits further investigation.

autoantibody, neuropathy, diabetes

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