SESSION TITLE: ARDS Posters
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Wednesday, October 28, 2015 at 01:30 PM - 02:30 PM
PURPOSE: ARDS is associated with neutrophil mediated inflammation in the lungs. Previously, we have shown that a collagen derived tri-peptide proline-glycine-proline (PGP), a neutrophil chemo attractant is elevated in patients with chronic diseases with neutrophilic predominant inflammation such as COPD and cystic fibrosis. However, it is unknown if PGP is elevated in ARDS. We hypothesized that levels of PGP are increased in ARDS as compared to cardiogenic edema and non- lung disease ventilated patients.
METHODS: Mini- bronchoalveolar lavage from 6 ARDS (A), 5 cardiogenic edema (C) and 5 non-lung disease (N) ventilated patients admitted to the intensive care unit of University of Alabama Hospital was collected on day 1 of mechanical ventilation. PGP, Leukotriene A4 hydroxylase (LTA4H) and myeloperoxidase (MPO) levels were measured using standard assays. Patient demographics, APACHE score, Pao2 to Fio2 (PF) ratio and outcomes were recorded. Results were expressed as means and proportions. One-way anova was used to compare means.
RESULTS: Average age of A, C, N patients was 59.5 (7.4), 44.5 (19) and 46.5(10) years respectively. Males comprised 50% in A, 20% in C and 60% in N. Mean APACHE score was 25.5 (2.8) in A, 12.5 (6.8) in C and 10.2 (8) in N. Mean PF was 149.5 (65.6) in A, 234.4(88.3) in C and 499(55) in N. Average length of mechanical ventilation in days was 10.5 (6.5) in A, 2.2 (2) in C and 2.4 (2.1) in N. Mortality in A was 66.6%, while C and N had no mortality. The mean PGP (ng/ml) level in A (2.63 (2.3)) was significantly higher than C (0.13(0.21)) and N (0.16 (0.24)) (p<0.01). Similarly, mean MPO (ng/ml) levels were significantly higher in A (5656.07 (3088.4)) as compared to C (1199.25 (2104.2)) and N (1580.5 (2527.1)) (p<0.02) suggesting elevated neutrophil burden in A. We also measured levels of LTA4H, an enzyme that degrades PGP. LTA4H levels (ng/mg protein) were higher in N (2.12(2.72)) and C (1.91(3.05)) as compared to A (0.59(0.77)) suggesting greater inhibition of PGP related neutrophilic inflammation in C and N.
CONCLUSIONS: PGP levels are elevated in ARDS as compared to cardiogenic edema and non-lung disease patients. Therefore it is plausible that PGP may be a regulator in neutrophil mediated inflammation in ARDS.
CLINICAL IMPLICATIONS: PGP can be used as a biomarker to distinguish ARDS from cardiogenic edema. In addition, it could also be used as a potential therapeutic target in ARDS. Larger studies are needed to validate this further.
DISCLOSURE: The following authors have nothing to disclose: Nirmal Sharma, Tarek Abdallah, Wilson King, amit gaggar, Xin Xu
No Product/Research Disclosure Information