Abstract
Background
Scientific evidence indicates that endothelial glycocalyx (EG) shedding contributes to the pathophysiological installation of acute respiratory distress syndrome (ARDS) after bacterial sepsis. The aim was to evaluate the EG shedding in ARDS installation after flu syndrome.
Methods
This cross-sectional study included patients with flu syndrome during the influenza outbreak divided into two groups: patients with and without ARDS. Healthy subjects without flu syndrome were included in a control group. We measured EG damage biomarkers (hyaluronan, syndecan-1) and endothelial cell injury biomarker (soluble thrombomodulin) during the first medical evaluation. Histological assessment of the perimeter of the hyaline membrane and the number of neutrophils infiltrated in the alveolar septum was performed in patients who died.
Results
ARDS group had 30 patients (44 ± 16 years old, 57% men), the non-ARDS group had 36 patients (39 ± 17 years old, 42% men), and the control group had 35 individuals (44 ± 9 years old, 51% men). Hyaluronan levels were significantly higher in the ARDS group than the two groups [31 ng/ml (interquartile range-IQR 12–56) vs. 5 ng/ml (IQR 3–10) vs. 5 ng/ml (IQR 2–8); p < 0.0001]. Hyaluronan levels above 19 ng/ml in patients with flu syndrome were associated with a significant increase in 28-day mortality rate: relative risk (RR): 6.95; (95% confidence interval 1.88–25.67); p = 0.0017. A positive correlation was observed between hyaline membrane perimeter and soluble thrombomodulin levels (r = 0.89; p = 0.05) as well as between the number of neutrophils in the alveolar septum and hyaluronan levels (r = 0.89; p = 0.05).
Conclusions
Evidence of EG shedding was found in ARDS established after flu syndrome.
Faculty Opinions recommendation of Recombinant thrombomodulin protects against LPS-induced acute respiratory distress syndrome via preservation of pulmonary endothelial glycocalyx.
