Abstract
BackgroundScientific 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.MethodsThis 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.ResultsARDS 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).ConclusionsEvidence of EG shedding was found in ARDS established after flu syndrome.
Highlights
Scientific evidence indicates that endothelial glycocalyx (EG) shedding contributes to the pathophysiological installation of acute respiratory distress syndrome (ARDS) after bacterial sepsis
This study aimed to investigate the occurrence of EG shedding through biomarkers of damage of this structure and biomarker of endothelial cell injury and its participation in ARDS establishment after flu syndrome
As we did not know the behavior of the hyaluronan levels in the intermediate group, in which we initially considered to have a middle level of hyaluronan, we decided to include at least double these initial number of patients (n = 24)
Summary
Scientific evidence indicates that endothelial glycocalyx (EG) shedding contributes to the pathophysiological installation of acute respiratory distress syndrome (ARDS) after bacterial sepsis. Respiratory viruses are endemic worldwide and usually cause benign and self-limiting disease Sometimes, they can reach the lower airway, especially the influenza virus, and trigger severe pneumonia associated with acute respiratory distress syndrome (ARDS) [1, 2]. They can reach the lower airway, especially the influenza virus, and trigger severe pneumonia associated with acute respiratory distress syndrome (ARDS) [1, 2] At times, another respiratory virus can emerge and cause epidemics, Endothelial glycocalyx (EG) is a carbohydrate-rich gelatinous layer that covers the vessels internally [4, 5]. This study aimed to investigate the occurrence of EG shedding through biomarkers of damage of this structure (hyaluronan and syndencan-1) and biomarker of endothelial cell injury (soluble thrombomodulin) and its participation in ARDS establishment after flu syndrome
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