Objective: Activation of endothelial cells is a critical step in the pathogenesis of acute respiratory distress syndrome (ARDS). Soluble endothelial selectin (sE-selectin), an endothelial cell-specific molecule that mediates leukocyte-endothelial cell adhesion has never been measured in the bronchoalveolar lavage fluid of critically ill patients. Based on the effects of alcohol on endothelial cell and alveolar-capillary barrier function, we hypothesized that chronic alcohol exposure may be associated with increased sE-selectin in ARDS patients.
Design: Prospective observational cohort study.
Setting: Medical and surgical intensive care units; an inpatient alcohol detoxification unit within university-affiliated hospitals.
Patients: A total of 20 ARDS patients (50% with chronic alcohol abuse); seven individuals with a history of chronic alcohol abuse.
Intervention: Patients underwent bronchoalveolar lavage within 72 hrs of ARDS diagnosis. Individuals with a history of chronic alcohol abuse underwent bronchoalveolar lavage within 7 days of their last alcoholic beverage. A history of chronic alcohol abuse was determined by a Short Michigan Alcohol Screening Test score of > or =3 or a history of an alcohol-related diagnosis. sE-selectin was measured in plasma and bronchoalveolar lavage.
Measurements and main results: Neither severity of illness nor at-risk diagnosis differed by alcohol history. sE-selectin levels in the plasma of ARDS patients who abused alcohol chronically were significantly elevated compared with nonalcoholic ARDS patients (181 ng/mL [56-328] vs. 32 ng/mL [14-55], p <.01). The bronchoalveolar lavage sE-selectin levels from the patients with ARDS and alcohol abuse were also significantly elevated compared with nonalcoholic ARDS patients (1.51 ng/mL [1.09-3.11] vs. 0.69 ng/mL [0.33-0.94], p <.002) and were higher than those measured in individuals with a history of chronic alcohol abuse but without ARDS (0.46 ng/mL [0.12-2.75], p =.15).
Conclusions: ARDS patients who chronically abuse alcohol have elevated concentrations of sE-selectin in both the plasma and epithelial lining fluid consistent with altered endothelial cell and alveolar-capillary barrier function.