Document Detail


Dexamethasone treatment of infants at risk for chronic lung disease: surfactant components and inflammatory parameters in airway specimens.
MedLine Citation:
PMID:  7808837     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The mechanisms explaining the beneficial effects of glucocorticoid in ventilator-dependent preterm infants are not known. In the present randomized trial, we evaluated the hypothesis that dexamethasone (DEX) treatment of small, preterm infants at risk for chronic lung disease favorably affects the surfactant system. Twenty-three ventilator-dependent infants, with a mean +/- SD gestational age of 26 +/- 2 wk and a mean birth weight of 836 +/- 173 g, received 1 wk of treatment with either DEX (dose 0.5 mg/kg/d) or placebo beginning at 2 wk of age. The airway specimens were analyzed for surfactant components, surface activity, surfactant inhibitors, and inflammatory mediators. The concentrations of these parameters in epithelial lining fluid were calculated using the urea method. DEX treatment decreased the concentration of nonsedimentable protein in epithelial lining fluid within 3 d (p < 0.05). The nonsedimentable fraction of airway specimens decreased the surface activity of surfactant as a function of protein concentration. At a constant protein concentration, the protein from placebo-treated infants inhibited the surface activity of human surfactant in vitro more than protein from DEX-treated infants (p < 0.05). DEX transiently increased the concentration of surfactant protein-A in epithelial lining fluid but had no effect on surface activity of the sedimentable surfactant complex or on concentrations of phosphatidylcholine, IL-1 beta, lactoferrin, or myeloperoxidase. We conclude that the acute beneficial effect of DEX treatment in preterm ventilator-dependent infants may in part be mediated through a decrease in the concentration of non-sedimentable protein and a decrease in the capacity of this protein to inhibit surface activity.
Authors:
M A Kari; K O Raivio; P Venge; M Hallman
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Publication Detail:
Type:  Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pediatric research     Volume:  36     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  1994 Sep 
Date Detail:
Created Date:  1995-02-02     Completed Date:  1995-02-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  387-93     Citation Subset:  IM    
Affiliation:
Children's Hospital, University of Helsinki, Finland.
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MeSH Terms
Descriptor/Qualifier:
Blood Proteins / metabolism
Chronic Disease
Dexamethasone / therapeutic use*
Female
Humans
Infant, Low Birth Weight
Infant, Newborn
Infant, Premature, Diseases / drug therapy*,  metabolism
Inflammation / metabolism
Interleukin-1 / metabolism
Lactoferrin / metabolism
Lung Diseases / drug therapy*,  metabolism
Male
Peroxidase / metabolism
Pulmonary Surfactants / antagonists & inhibitors,  chemistry
Risk Factors
Trachea / metabolism
Treatment Outcome
Chemical
Reg. No./Substance:
0/Blood Proteins; 0/Interleukin-1; 0/Lactoferrin; 0/Pulmonary Surfactants; 50-02-2/Dexamethasone; EC 1.11.1.7/Peroxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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