Tracheobronchial aspirate proinflammatory cytokines: early predictors of chronic lung disease in neonates with respiratory distress syndrome

ABSTRACT

The objectives of the present study were to investigate if early measurements of proinflammatory cytokines in tracheobronchial aspirate fluid from neonates with respiratory distress syndrome [RDS] could be used to early predict chronic lung disease [CLD]. This is in comparison with other risk factors including gestational age, birth weight, prenatal steroid, mode of delivery, duration of exposure to FiO[2] >0.21, peak inspiratory pressure [PIP] and duration of ventilatory support, air leaks, patent ductus arteriosus [PDA], and intraventricular hemorrhage [IVH]. Thirty-six preterm infants less than 34 weeks of gestation with RDS were mechanically ventilated and days 2 and 7 - measurements of concentrations of tumor necrosis factor-alpha [TNF-alpha] and the interleukins IL-1beta, IL-6, and IL-8 were made, using enzyme immunoassay techniques. Echo-Doppler and head ultrasonography studies were done for each patient. Each patient was followed-up for 28 days. Ten patients developed CLD, six patients died before the elapse of 28 days, and 20 patients experienced uncomplicated course of RDS. Infants who developed CLD had significantly increased concentrations of TNF-alpha, IL-1beta, IL-8, and IL-6 on days 2 that persist by day 7. TNF-alpha, IL-6, IL-8, and IL-1beta concentrations correlated significantly with lower gestational age, birth weight, time spent on a ventilator, duration of supplemental oxygen, maximal PIP, symptomatic PDA, and appearance of air leak. IL-6 cut-off point level of 650 pg/ml at day 2 predicts CLD with accuracy of 100%, and IL-1beta cut-off point level of 165 pg/ml at day 2 predicts CLD with accuracy of 100%. In conclusion, increased concentrations of tracheobronchial aspirate fluid proinflammatory cytokines could be the most valuable early predictor of CLD and will assist in selecting infants for early interventions including corticosteroid treatment or more selective blockage of components of inflammation