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Evaluation of Pre-Treatment and Post-Treatment S100B, Oxidant and Antioxidant Capacity in Children with Diabetic Ketoacidosis

OBJECTIVE: The study aimed to evaluate the pre-treatment and post-treatment oxidant capacity, antioxidant capacity and S100B protein levels in cases of diabetic ketoacidosis (DKA). METHODS: The study included 49 pediatric patients diagnosed with DKA and a control group comprising 49 healthy children...

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Detalles Bibliográficos
Autores principales: Kaya, Cemil, Ataş, Ali, Aksoy, Nurten, Kaya, Esra Celen, Abuhandan, Mahmut
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Galenos Publishing 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4563181/
https://www.ncbi.nlm.nih.gov/pubmed/26316432
http://dx.doi.org/10.4274/jcrpe.1716
Descripción
Sumario:OBJECTIVE: The study aimed to evaluate the pre-treatment and post-treatment oxidant capacity, antioxidant capacity and S100B protein levels in cases of diabetic ketoacidosis (DKA). METHODS: The study included 49 pediatric patients diagnosed with DKA and a control group comprising 49 healthy children. Blood samples were obtained after confirmation of the DKA diagnosis and also after treatment. S100B, total oxidant (TOL) and total antioxidant levels (TAL) were measured and the oxidative stress index (OSI) was calculated. RESULTS: When the pre-treatment and post-treatment values of patients with DKA were compared with those of the healthy control group, the S100B level, TOL, TAL and OSI were found to be significantly higher in the diabetes group (p<0.001). Pre-treatment TOL and TAL were also significantly higher than post-treatment levels (p<0.001), while no statistically significant difference was found in the S100B levels or the OSI (p>0.05). CONCLUSION: We believe that long-term exposure to high blood glucose concentrations leads to an increase in TOL in patients with DKA and that the neurotransmitter changes that develop in response to this exposure lead to an increase in S100B levels, which is an indicator of neuronal damage.