Acute Respiratory Distress Syndrome, ARDS Clinical Trial
The acute respiratory distress syndrome (ARDS), characterized by alveolar flooding with
protein-rich pulmonary edema fluid, is one of the most common disease in the intensive care
unit (ICU) throughout the world. In recent years, much effort has been focused on the
biological markers for their potential values to diagnose ARDS and outcomes.
ARDS is generally accompanied by the disruption in alveolar-capillary barrier permeability,
which subsequently caused an influx of neutrophils into the interstitium and alveolar space.
It was reported that the aggregation, adhesion activation and release proteases of
neutrophils are the key pathogenesis of ARDS pulmonary edema. Neutrophil Elastase (HNE), the
most crucial protease generated in neutrophil azurophilic granules, plays an important role
in various inflammations, especially the lung injury. The destructive action of HNE on
almost all extracellular matrix influences cell signaling through cleavage of surface
receptors. Once released in circulation, HNE is rapidly inactivated by conjugation with PI3.
This local inhibitor reduces HNE mediated tissue injury and inflammation. Thus, the
investigators plan to conduct a cohort study with repeated measures to examine the
diagnostic and prognostic value of HNE and PI3 for ARDS.
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Observational Model: Cohort, Time Perspective: Prospective