Abstract
Background. Considering that most diagnostic tests for diabetic peripheral polyneuropathy (DPN) are not suitable for use in childhood, resulting in low diagnostic accuracy of this complication, there is a need to identify reliable and simple markers for early detection and monitoring of diabetic polyneuropathy progression in children. Purpose: to study the content of fetuin A, gamma-aminobutyric acid (GABA), S100 protein and copeptin in the blood serum of children with type 1 diabetes mellitus and determine their role in the development of diabetic peripheral polyneuropathy. Materials and methods. We examined 63 children with type 1 diabetes aged 10 to 17 years. Group 1 included 26 patients without signs of neuropathy, group 2 consisted of 37 patients with diabetic peripheral polyneuropathy. The control group included 29 children representative in terms of age and gender without carbohydrate metabolism disorders. The serum levels of fetuin A, gamma-aminobutyric acid, S100 protein, and copeptin were determined by enzyme-linked immunosorbent assay using commercial kits. Results. It has been proven that in children with type 1 diabetes who did not have DPN, there was a 1.6-fold increase in fetuin A and a 2.4-fold increase in GABA compared to the control group (p < 0.05). With the development of DPN, there was a decrease in both fetuin A and GABA. A significant statistical increase in the serum level of S100 and copeptin was found in children with DPN, while in the group without signs of DPN, their values did not statistically differ from the control group (p > 0.05). An increase in the severity of neurological deficit was inversely related to the level of fetuin A (r = –0.40; p < 0.05) and GABA (r = –0.45; p < 0.05) and positively correlated with the serum content of S100 protein (r = 0.66; p < 0.05) and copeptin (r = 0.68; p < 0.05). Conclusions. A comprehensive study of fetuin, GABA, S100 protein and copeptin can act as an additional objective marker for the development of DPN in children with type 1 diabetes mellitus and will allow for the objectification and improvement of the diagnosis of this complication.
Published Version
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