ESPE2014 Poster Presentations Diabetes (11 abstracts)
aDepartment of Pediatric Endocrinology, University of Harran, Sanliurfa, Turkey; bDepartment of Biochemistry, University of Harran, Sanliurfa, Turkey
Background: Diabetic ketoacidosis is a serious condition with high rates of morbidity and mortality in children with type 1 diabetes mellitus. Calcium-binding protein S100B is a cell damage marker glycopeptide that is mainly produced by astrocytes. Oxidative stress might be defined as an imbalance between anti-oxidative defense of the body and free radical production responsible for peroxidation of lipid layer of cell walls.
Objective and hypotheses: In patients with diabetic ketoacidosis, high blood glucose concentration may increase oxidative stress and consequent changes in neurotransmitter by which may increase the level of S100B. In this study we aimed to investigate S100B protein levels, oxidant and antioxidant capacity in children with diabetic ketoacidosis.
Methods: 49 healthy children and 49 children with diabetic ketoacidosis included into this study. Peripheral venous bloods were taken for tests during diabetic ketoacidosis and after recover diabetic ketoacidosis. Measurement of serum S100B was performed by ELISA Kits. Total antioxidant status (TAS), Total oxidant status (TOS), and oxidative stress index (OSI) were studied at peripheral venous blood by Erel method.
Results: Comparing pretreatment and post-treatment of TAS, TOS, S100B levels were significantly higher in patients with diabetic ketoacidosis than healthy control group (P<0.05). There was no significant difference in the levels of S100B and OSI (P>0.05). In our study there was also a positive correlation between S100B with the TOS and OSI values (respectively r: 0.235, r: 0.244; P: 0.006, P: 0.005).
Conclusions: In diabetic ketoacidosis, increase of oxidative stress and S100B may be depending on high glucose level. Increasing concentrations of these factors in blood may be therefore indicative for either neuronal damage, impaired blood brain barrier function, or both.