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Soluble Intercellular Adhesion Molecule-1, Macrophage Migration Inhibitory Factor and Plasminogen Activator Inhibitor-1 as Predictors of Outcome in Acute Respiratory Distress Syndrome

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A1806 - Soluble Intercellular Adhesion Molecule-1, Macrophage Migration Inhibitory Factor and Plasminogen Activator Inhibitor-1 as Predictors of Outcome in Acute Respiratory Distress Syndrome
Author Block: E. Vrigkou1, M. Alepaki2, A. Tsantes3, V. Tsagkari1, K. Ntai1, A. Pappas1, D. Konstantonis1, A. Armaganidis1, I. Tsagkaris1; 12nd Department of Critical Care, Attikon University Hospital, Athens, Greece, 22nd Department of Cytology, Attikon University Hospital, Athens, Greece, 3Laboratory of Hematology and Blood Bank Unit, Attikon University Hospital, Athens, Greece.
Rationale: Acute Respiratory Distress Syndrome (ARDS) is an acute lung process characterized by alveolar epithelial and lung endothelial injury, dysregulated inflammation and coagulation abnormalities. Soluble intercellular adhesion molecule-1 (sICAM-1) and macrophage migration inhibitory factor (MIF) are cytokines modulating a variety of inflammatory and immune-mediated mechanisms. Plasminogen activator inhibitor 1 (PAI-1) is a coagulation protein with a primary role in inhibiting fibrinolysis. The aim of this study was to investigate the value of circulating as well as bronchoalveolar lavage fluid (BALF) sICAM-1, MIF and PAI-1 levels as predictors of outcome in mechanically ventilated patients with ARDS.
Methods: Fifty consecutive patients with ARDS, ventilated according to NIH protocol, were enrolled within 48 hours of recognition of their disease. All patients underwent bronchoalveolar lavage upon
enrolment. A multiplex bead-based assay was used for the determination of the concentrations of sICAM, MIF and PAI-1 in the serum and BALF. The primary outcome was mortality at 28 days. Secondary outcomes were days of unassisted ventilation and days with organ failure other than lung, during the 28-day study period.
Results: Non-survivors (n= 27) didn’t present significant differences to survivors (n= 23) regarding sex (11♀-16♂ vs 9♀-14♂), but were younger in age (60.2 ± 17.5 vs 68.3 ± 9.5), with higher SOFA scores (8.9 ± 3.4 vs 7.5 ± 3.2) and lower PaO2/FiO2 indexes (144.8 ± 59.3 vs 161.6 ± 59.9). Our results showed that sICAM-1 values in serum were significantly elevated in non-survivors compared to survivors (305.3 ng/ml ± 140.5 vs 224.3 ± 80.5, p= 0.03). Respectively, non-survivors presented higher BALF sICAM-1 levels in relation to survivors (84.7 ng/ml ± 102 vs 24.6 ± 30.7, p= 0.009). PAI-1 serum measurements in non-survivors were marginally non-significantly elevated when compared to survivors (146.5 ng/ml ± 185.2 vs 70.5 ± 37.3, p= 0.06), whereas BALF PAI-1 levels didn’t present significant differences between the two groups. No significant variations were determined in serum and BALF MIF values. Finally, non-survivors presented with fewer days of unassisted ventilation and more days with organ failure other than lung compared to survivors.
Conclusions: Our findings suggest that sICAM-1 levels may be increased in serum and the alveolar compartment of patients with ARDS and this might be associated with increased mortality. Serum PAI-1 measurements were found to be marginally not significantly different between survivors and not survivors.
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