Glutathione peroxidase and superoxide dismutase as markers of brain dysfunction in adolescents with diabetic ketoacidosis

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Introduction. Diabetic ketoacidosis (DKA) is the most prevalent and severe acute complication of type 1 diabetes mellitus (DM) in children and adolescents. Oxidative stress (OS) is viewed on the one hand as a possible pathophysiological element in the development of this complication, and on the other, as an important factor that triggers the development of cerebral insufficiency in patients with type 1 DM.Aim: to study the content of antioxidant enzymes in adolescents with type 1 DM in the setting of DKA and determine the correlation between the concentration of glutathione peroxidase (GP) and superoxide dismutase (SOD) and brain dysfunction after the manifestation of DKA.Materials and methods. The study involved 52 adolescents (mean age − (16.7±1.25) years), of whom 26 were patients with type 1 DM complicated by DKA (study group; duration of disease − (6.5±0.46) years) and 26 were apparently healthy adolescents (control group). Cognitive functioning was assessed using the Montreal Cognitive Assessment (MoCA) test. Concentration of GP and SOD was assessed in serum samples by ELISA. Mann-Whitney test was used to assess differences between means, and Spearman’s coefficient was used to calculate correlations.Results. Assessment using the MoCA tool showed a statistically significant cognitive decline in adolescents who had an episode of DKA (p = 0.0001). Another statistically significant finding in DKA was the lower mean levels of both GP (p = 0.0031) and SOD (p = 0.0173). Negative correlation was discovered between values obtained in the MoCA test and duration of disease and number of hospital admissions with DKA, and between GP levels and number of admissions with DKA, as reflected in patient history. Positive correlation was discovered between GP and SOD levels and values obtained in the MoCA test.Discussion. Patients were found to have decreased antioxidant defense, along with brain dysfunction, after the manifestation of DKA. DKAassociated impairment of antioxidant defense is one of the pathophysiological mechanisms underpinning the development of cognitive dysfunction in adolescents with type 1 DM. Conclusion GP and SOD can be viewed as markers of DKA-associated brain dysfunction in patients with type 1 DM.