Persistent elastase/proteinase inhibitor imbalance during prolonged ventilation of infants with bronchopulmonary dysplasia: evidence for the role of nosocomial infections

• Published in: Pediatric research Vol. 26; no. 4; pp. 351 - 355
• Main Authors: WALTI, H, TORDET, C, GERBAUT, L, SAUGIER, P, MORIETTE, G, RELIER, J. P
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.10.1989
• Subjects: alpha 1-Antitrypsin - metabolism; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Bronchoalveolar Lavage Fluid - metabolism; Bronchopulmonary Dysplasia - complications; Bronchopulmonary Dysplasia - metabolism; Bronchopulmonary Dysplasia - therapy; Cross Infection - complications; Cross Infection - metabolism; Emergency and intensive care: neonates and children. Prematurity. Sudden death; Humans; Infant, Low Birth Weight - metabolism; Infant, Newborn; Intensive care medicine; Medical sciences; Pancreatic Elastase - metabolism; Prospective Studies; Respiration, Artificial; Serum Albumin - metabolism; Human; Infection; Pathophysiology; Respiratory disease; Proteinase; Enzyme inhibitor; Bronchopulmonary dysplasia; Infant; Respiratory intensive care; Elastase; Artificial ventilation
• ISSN: 0031-3998; 1530-0447
• DOI: 10.1203/00006450-198910000-00013

Acute imbalance between elastase and alpha-1-proteinase inhibitor (alpha 1Pi) may contribute to the development of bronchopulmonary dysplasia (BPD). The question of whether such an imbalance persists in BPD infants still requiring mechanical ventilation after 4 wk of life has not been previously addressed. We studied 14 infants still on mechanical ventilation at 4 wk of age: nine had BPD and five did not. Weekly (4 to 9 wk) serum and bronchoalveolar lavage (BAL) specimens were taken. alpha 1Pi and alpha-2-macroglobulin were measured in serum and BAL by immunoturbidimetric assay. BAL elastase activity was measured by cleavage of a synthetic substrate and expressed as ng of porcine pancreatic elastase equivalent. Infants with BPD had higher levels of serum alpha 1Pi and alpha-2-macroglobulin than those without BPD. In contrast, the corresponding BAL levels were either similar or even decreased (alpha 1Pi). Moreover, there was a 3-fold increase in elastase-1Pi imbalance expressed as the BAL ng of porcine pancreatic elastase equivalent/2 alpha 1Pi ratio. The role of nosocomial infections was evident in a subgroup of 11 infected BAL aspirates in BPD infants. In such cases we found a 3-fold increase in the BAL ng of porcine pancreatic elastase equivalent/alpha 1Pi ratio as compared to 35 noninfected BAL in BPD infants. These data suggest a persistent alveolitis with imbalance between elastase and proteinase inhibitors in prolonged severe BPD. Such an imbalance is, in part, explained by a local destruction and/or inactivation of alpha 1Pi. Our results also emphasize the increase in proteolysis with nosocomial pneumonia.