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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2014
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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 |
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author | Demir, Nihat Ece, İbrahim Peker, Erdal Kaba, Sultan Ustyol, Lokman Balahoroğlu, Ragip Tuncer, Oğuz |
author_facet | Demir, Nihat Ece, İbrahim Peker, Erdal Kaba, Sultan Ustyol, Lokman Balahoroğlu, Ragip Tuncer, Oğuz |
author_sort | Demir, Nihat |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4283821 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-42838212015-01-08 Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants Demir, Nihat Ece, İbrahim Peker, Erdal Kaba, Sultan Ustyol, Lokman Balahoroğlu, Ragip Tuncer, Oğuz Med Sci Monit Clinical Research 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. International Scientific Literature, Inc. 2014-12-26 /pmc/articles/PMC4283821/ /pubmed/25542161 http://dx.doi.org/10.12659/MSM.892166 Text en © Med Sci Monit, 2014 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Clinical Research Demir, Nihat Ece, İbrahim Peker, Erdal Kaba, Sultan Ustyol, Lokman Balahoroğlu, Ragip Tuncer, Oğuz Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title | Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title_full | Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title_fullStr | Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title_full_unstemmed | Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title_short | Impact of Patent Ductus Arteriosus and Subsequent Therapy with Ibuprofen on the Release of S-100B and Oxidative Stress Index in Preterm Infants |
title_sort | impact of patent ductus arteriosus and subsequent therapy with ibuprofen on the release of s-100b and oxidative stress index in preterm infants |
topic | Clinical Research |
url | 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 |
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