SECRETORY LEUKOCYTE PROTEASE INHIBITOR AND LUNG INFLAMMATION IN DEVELOPING BRONCHOPULMONARY DYSPLASIA

Citation
Kl. Watterberg et al., SECRETORY LEUKOCYTE PROTEASE INHIBITOR AND LUNG INFLAMMATION IN DEVELOPING BRONCHOPULMONARY DYSPLASIA, The Journal of pediatrics, 125(2), 1994, pp. 264-269
Citations number
26
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00223476
Volume
125
Issue
2
Year of publication
1994
Pages
264 - 269
Database
ISI
SICI code
0022-3476(1994)125:2<264:SLPIAL>2.0.ZU;2-S
Abstract
Objective: To investigate secretory leukocyte protease inhibitor (SLPI ) concentrations in tracheal lavage fluids of neonates with an endotra cheal tube in place during the first month of life, and to evaluate th e relationship of SLPI to neutrophil counts and elastase activity in p atients in whom bronchopulmonary dysplasia (BPD) developed versus thos e in whom it did not. Design: A prospective, inception cohort study. S etting: University children's hospital neonatal intensive care unit. P atients: Fifty-three neonates who weighed <2000 gm at birth, and who h ad an endotracheal tube in place, were enrolled. Forty-one patients su rvived to 28 days; BPD developed in 24 but not in 17 patients. Main ou tcome measures: Tracheal lavage was performed on days 1, 2, 4, 7, 14, 21, and 28, and analyzed for neutrophils, elastase activity, and SLPI. Results were evaluated longitudinally for 28 days, and were compared between BPD and no-BPD groups during the first week, Results: SLPI con centrations increased significantly for all patients during the study period. During the first week, SLPI concentrations were similar betwee n BPD and no-BPD groups; neutrophil counts and elastase activity were higher in the BPD group. Conclusions: Patients in whom BPD ultimately developed had early evidence of increased pulmonary inflammation and a significantly less favorable protease-antiprotease balance. If elasta se-induced injury contributes to the development of BPD, early therapy with recombinant SLPI might be beneficial by increasing the antielast ase capacity of epithelial lining fluid.