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Inflammatory mediators in premature ...

Carlson, Cheryl Ann.

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Inflammatory mediators in premature infants with surfactant deficiency and dysfunction.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Inflammatory mediators in premature infants with surfactant deficiency and dysfunction./
作者:	Carlson, Cheryl Ann.
面頁冊數:	117 p.
附註:	Adviser: Gail Stuart.
Contained By:	Dissertation Abstracts International68-08B.
標題:	Health Sciences, Medicine and Surgery. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3280916
ISBN:	9780549189381

Inflammatory mediators in premature infants with surfactant deficiency and dysfunction.
Carlson, Cheryl Ann.

Inflammatory mediators in premature infants with surfactant deficiency and dysfunction. - 117 p.

Adviser: Gail Stuart.

Thesis (Ph.D.)--Medical University of South Carolina, 2007.

The inflammatory process is the response of the body to defend against pathogens and toxic substances, and repair damaged tissue. In the lungs, damage to the pulmonary capillary endothelium and epithelium results in capillary leak, exudation of plasma and plasma proteins into the alveolar space and the release of pro-inflammatory mediators. The acute inflammatory response associated with secondary respiratory failure can lead to severe lung injury resulting in impaired gas exchange, and possibly death.

ISBN: 9780549189381Subjects--Topical Terms:

1017756
Health Sciences, Medicine and Surgery.

Inflammatory mediators in premature infants with surfactant deficiency and dysfunction.
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245 1 0 $a Inflammatory mediators in premature infants with surfactant deficiency and dysfunction.
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502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2007.
520 $a The inflammatory process is the response of the body to defend against pathogens and toxic substances, and repair damaged tissue. In the lungs, damage to the pulmonary capillary endothelium and epithelium results in capillary leak, exudation of plasma and plasma proteins into the alveolar space and the release of pro-inflammatory mediators. The acute inflammatory response associated with secondary respiratory failure can lead to severe lung injury resulting in impaired gas exchange, and possibly death.
520 $a Surfactant administration in premature infants who develop a secondary respiratory decompensation may decrease the inflammatory cascade and protect the lungs from fibrosis and edema. A prospective, pilot study was done to study the effect of surfactant on cytokine response in tracheal aspirates. A secondary data analysis was performed looking at respiratory severity scores and the inflammatory mediators.
520 $a Entry criteria included infants who were > 7 days of age, qualifying if they had a secondary respiratory decompensation, after recovery from primary RDS. Infants meeting all entry criteria received either Curosurf or Survanta within four hours of the qualifying decompensation and again 12 hours later. Oxygen, ventilatory parameters, blood gas results and tracheal aspirate samples were collected prior to, and 12 and 24 hours after dosing.
520 $a Twenty neonates qualified for secondary surfactant administration and 10 had tracheal aspirates collected at the 3 time points. There were trends toward decreasing pro-inflammatory cytokines after surfactant administration. Surfactant dosing seemed to disrupt the correlation of pro-inflammatory cytokines, suggesting that inflammatory cytokines are affected differently.
520 $a The Respiratory Severity Score (RSS) and Modified Ventilatory Index (MVI) have been studied in this group of infants. The ability to use clinical data in an objective scoring system that correlates with the inflammatory process in the lungs would be advantageous in deciding when and which treatment options were most appropriate. Based on this study, MVI scores seemed to be a better indicator of changes in inflammatory mediators, and maybe a better predictor of on-going inflammation and risk of CLD. Further randomized controlled trials are needed to confirm these preliminary results.
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