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Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants

BACKGROUND: Hemodynamically significant patent ductus arteriosus (hsPDA) leads to injury in tissues/organs by reducing perfusion of organs and causing oxidative stress. The purpose of this study was to evaluate the oxidant/antioxidant status in preterm infants with hsPDA by measuring the total antio...

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Detalles Bibliográficos
Autores principales: Demir, Nihat, Ece, İbrahim, Peker, Erdal, Kaba, Sultan, Ustyol, Lokman, Balahoroğlu, Ragip, Tuncer, Oğuz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283821/
https://www.ncbi.nlm.nih.gov/pubmed/25542161
http://dx.doi.org/10.12659/MSM.892166
Descripción
Sumario:BACKGROUND: Hemodynamically significant patent ductus arteriosus (hsPDA) leads to injury in tissues/organs by reducing perfusion of organs and causing oxidative stress. The purpose of this study was to evaluate the oxidant/antioxidant status in preterm infants with hsPDA by measuring the total antioxidant capacity and total oxidant status and to assess neuronal damage due to oxidant stress related to hsPDA. MATERIAL/METHODS: This prospective study included 37 low-birth-weight infants with echocardiographically diagnosed hsPDA treated with oral ibuprofen and a control group of 40 infants without PDA. Blood samples were taken from all infants, and than the total antioxidant capacity (TAC), total oxidant status (TOS), and S-100B protein levels were assessed and oxidative stress index was calculated before and after therapy. RESULTS: The mean pre-therapy TOS level and oxidative stress index (OSI) value of the patients with hsPDA were significantly higher, but TAC level was lower than in the control group. There were no statistically significant differences in the mean post-therapy values of TOS, TAC, OSI, and S-100B protein between the two groups. CONCLUSIONS: hsPDA may cause cellular injury by increasing oxidative stress and damaging tissue perfusion; however the brain can compensate for oxidative stress and impaired tissue perfusion through well-developed autoregulation systems to decrease tissue injury.