Prognostic value of epithelial neutrophil activating peptide 78 and monokine induced by IFNγ in bronchoalveolar lavage fluid in critically ill pediatric patients with acute respiratory distress syndrome

Introduction

Diffuse alveolar damage (DAD) is the histopathological hallmark of acute respiratory distress syndrome (ARDS). DAD is due, in part, to dysregulated angiogenesis, with over-expression of angiogenic and downregulation of angiostatic chemokines. The objective of this study was to measure the levels of epithelial neutrophil activating peptide 78 (ENA78) as an angiogenic chemokine and monokine induced by IFNγ (MIG) as an angiostatic chemokine in bronchoalveolar lavage fluid of critically ill children with ARDS to determine the prognostic value of the ENA78/MIG ratio in assessing illness severity and patient outcome.

Methods

The study included 35 mechanically ventilated pediatric patients with ARDS and 28 mechanically ventilated patients due to nonpulmonary causes as a control group with mean age 16.5 ± 10.2 and 29.1 ± 8.1 months, respectively. They were subjected to fibroaptic bronchoscopic examination and bronchoalveolar lavage was done to estimate the ENA-78 and MIG levels using the ELISA technique.

Results

Both ENA-78 and MIG levels were found to be significantly higher among patients versus controls (P < 0.01) (390.3 ± 159.7 vs. 80.3 ± 17.6 pg/ml and 235.6 ± 92 vs. 91.0 ± 18.9 pg/ml, respectively). ENA-78 was found to be significantly higher among nonsurvivors, while MIG was significantly lower among nonsurvivors in comparison with the survivors (P < 0.01) (455.3 ± 142 vs. 277.8 ± 29.1 pg/ml and 186.3 ± 43 vs. 359.0 ± 56.4 pg/ml, respectively). Applying a receiver operating characteristic curve indicated that ENA78/MIG ratio was the best discriminator between survivors and nonsurvivors at cutoff value 1.02 with 100% sensitivity and specificity.

Conclusion

Imbalance between angiogenic and angiostatic chemokines is the determining factor of ARDS patients' outcome. Future studies to investigate therapeutic modalities to enhance angiostatic factors or inhibit angiogenesis to delay diffuse alveolar damage and improve the outcome are recommended.