Soluble intercellular adhesion molecule-1 and clinical outcomes in patients with acute lung injury

Abstract

Objective: To determine if levels of soluble intercellular adhesion molecule-1 (sICAM-1), a marker of alveolar epithelial and endothelial injury, differ in patients with hydrostatic pulmonary edema and acute lung injury (ALI) and are associated with clinical outcomes in patients with ALI.

Design, setting, and participants: Measurement of sICAM-1 levels in (1) plasma and edema fluid from 67 patients with either hydrostatic pulmonary edema or ALI enrolled in an observational, prospective single center study, and (2) in plasma from 778 patients with ALI enrolled in a large multi-center randomized controlled trial of ventilator strategy.

Results: In the single-center study, levels of sICAM-1 were significantly higher in both edema fluid and plasma (median 938 and 545 ng/ml, respectively) from ALI patients compared to hydrostatic edema patients (median 384 and 177 ng/ml, P < 0.03 for both comparisons). In the multi-center study, higher plasma sICAM-1 levels were associated with poor clinical outcomes in both unadjusted and multivariable models. Subjects with ALI whose plasma sICAM-1 levels increased over the first 3 days of the study had a higher risk of death, after adjusting for other important predictors of outcome (odds ratio 1.48; 95% CI 1.03-2.12, P = 0.03).

Conclusions: Both plasma and edema fluid levels of sICAM-1 are higher in patients with ALI than in patients with hydrostatic pulmonary edema. Higher plasma sICAM-1 levels and increasing sICAM-1 levels over time are associated with poor clinical outcomes in ALI. Measurement of sICAM-1 levels may be useful for identifying patients at highest risk of poor outcomes from ALI.

Fig. 1

Boxplot summary of edema fluid (a) and plasma (b) levels in patients with hydrostatic pulmonary edema (n = 16) and ALI/ARDS (n = 51) from the single-center study. Edema fluid sICAM-1 levels were significantly higher in subjects with ALI (median 938 ng/ml, IQR 675–1743) compared to subjects with hydrostatic pulmonary edema (median 384 ng/ml, IQR 217–801) (a; P value for comparison 0.004). Plasma sICAM-1 levels demonstrated a similar pattern [b; median in ALI/ARDS (545 ng/ml, IQR 232–1330) vs. median in hydrostatic (177 ng/ml, IQR 137–703; P = 0.021)]