Epidemiology and outcome of acute lung injury in European intensive care units

Brun‐Buisson, Christian; Minelli, Cosetta; Bertolini, Guido; Brazzi, Luca; Pimentel, Jorge; Lewandowski, K.; Bion, Julian; Romand, Jacques-André; Villar, Jesús; Thorsteinsson, Adalbjörn; Damas, Pierre; Armaganidis, Apostolos; Lemaire, François

doi:10.1007/s00134-003-2022-6

Cited by 552 publications

(340 citation statements)

References 41 publications

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“…The discrepancy of basic diseases between the ARDS and non‐ARDS group might limit the clinical application of this study. In addition, the mortality of ARDS group in this study seems to be higher than other reported studies 1, 2, 3. This is probably due to the heterogeneity of different study populations.…”

Section: Discussioncontrasting

confidence: 60%

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Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome

Lin

Zhang

Wang

et al. 2017

Clinical Laboratory Analysis

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BackgroundAcute respiratory distress syndrome (ARDS) is a critical condition characterized by bilateral pulmonary infiltrates and severe hypoxemia. This study aimed to evaluate the diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with ARDS.MethodsIn this retrospective observational study, 83 patients with ARDS and 129 non‐ARDS patients on ICU admission were enrolled. The differences in serum CC16 and other laboratory indicators between two groups were analyzed. The sensitivity, specificity, positive and negative predictive values, and accuracy of CC16 as a diagnostic marker on ICU admission were determined by receiver operating characteristic (ROC) curve analysis. The correlation between serum CC16 levels and the severity of ARDS as quantified by PaO2/FiO2 ratio were further assessed. CC16 levels were compared between survivors and non‐survivors. The relationships between CC16 levels and duration of ICU and hospitalization were evaluated.ResultsThe serum CC16 levels in ARDS patients were significantly higher than that in non‐ARDS patients (54.44±19.62 vs 24.13±12.32 ng/mL, P=.001). ROC analysis showed that the sensitivity, specificity, positive predictive value, and negative predictive value were 90.4%, 79.8%, 74.2%, and 92.8%, respectively, when the cut‐off value was set at 33.3 ng/mL. CC16 levels were correlated with the severity of ARDS. The serum CC16 levels were significantly greater in non‐survivors than in survivors from the ARDS group. CC16 levels were associated with ICU stay but not hospital stay.Conclusions CC16 may serve as a diagnostic and stratification marker for ARDS. However, it provided limited prognostic information for ARDS.

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Section: Discussioncontrasting

confidence: 60%

“…Acute respiratory distress syndrome (ARDS), characterized by permeability pulmonary edema and refractory hypoxemia, has an enormous effect on both morbidity and mortality 1, 2, 3. The Berlin definition is widely accepted for diagnosing ARDS, and the diagnosis is predominantly based on oxygenation index and chest X‐ray 4.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome

Lin

Zhang

Wang

et al. 2017

Clinical Laboratory Analysis

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“…Because pulmonary inflammation precedes the onset of clinically defined ARDS, the identification of factors that can accelerate or augment inflammation in the pathogenesis of ARDS could lead to new therapeutic approaches to limit disease incidence and reduce mortality. Patients frequently develop ALI after admission to the hospital (2)(3)(4)(5), implying a possibility that potentially modifiable in-hospital exposures could contribute to the development of ALI in predisposed hosts. Supplemental oxygen (40-60%) comprises one such exposure (4)(5)(6).…”

mentioning

confidence: 99%

Macrophage A2A Adenosinergic Receptor Modulates Oxygen-Induced Augmentation of Murine Lung Injury

Aggarwal¹,

D’Alessio²,

Eto³

et al. 2013

Am J Respir Cell Mol Biol

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Acute respiratory distress syndrome (ARDS) causes significant morbidity and mortality. Exacerbating factors increasing the risk of ARDS remain unknown. Supplemental oxygen is often necessary in both mild and severe lung disease. The potential effects of supplemental oxygen may include augmentation of lung inflammation by inhibiting antiinflammatory pathways in alveolar macrophages. We sought to determine oxygen-derived effects on the anti-inflammatory A2A adenosinergic (ADORA2A) receptor in macrophages, and the role of the ADORA2A receptor in lung injury. Wild-type (WT) and ADORA2A2/2 mice received intratracheal lipopolysaccharide (IT LPS), followed 12 hours later by continuous exposure to 21% oxygen (control mice) or 60% oxygen for 1 to 3 days. We measured the phenotypic endpoints of lung injury and the alveolar macrophage inflammatory state. We tested an ADORA2A-specific agonist, CGS-21680 hydrochloride, in LPS plus oxygen-exposed WT and ADORA2A 2/2 mice. We determined the specific effects of myeloid ADORA2A, using chimera experiments. Compared with WT mice, ADORA2A2/2 mice exposed to IT LPS and 60% oxygen demonstrated significantly more histologic lung injury, alveolar neutrophils, and protein. Macrophages from ADORA2A 2/2 mice exposed to LPS plus oxygen expressed higher concentrations of proinflammatory cytokines and cosignaling molecules. CGS-21680 prevented the oxygen-induced augmentation of lung injury after LPS only in WT mice. Chimera experiments demonstrated that the transfer of WT but not ADORA2A 2/2 bone marrow cells into irradiated ADORA2A2/2 mice reduced lung injury after LPS plus oxygen, demonstrating myeloid ADORA2A protection. ADORA2A is protective against lung injury after LPS and oxygen. Oxygen after LPS increases macrophage activation to augment lung injury by inhibiting the ADORA2A pathway.

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“…Although many therapeutic strategies have been developed clinically [1,2,3], the mortality and morbidity associated with acute respiratory distress syndrome (ARDS) remains very high [4]. Since acute lung injury is nonhomogenous [5], some lung areas are less affected and therefore more compliant.…”

Section: Introductionmentioning

confidence: 99%

Response of Alveolar Type II Epithelial Cells to Mechanical Stretch and Lipopolysaccharide

Ning

Wang²

2007

Respiration

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Background: Although many therapeutic strategies have been developed clinically, the mortality associated with acute respiratory distress syndrome remains very high. Objectives: In this research, we used a cytomechanical method to elucidate the reason for this. Methods: A549 cells were stimulated with lipopolysaccharide (LPS; 1 or 100 ng/ml) and/or mechanical stretch (5, 15, 30%) in varying frequency (0.2, 0.5, 1 Hz) at indicated time (1, 2, 4 h). Real time PCR and enzyme-linked immunosorbent assay were used to measure mRNA and protein levels of IL-8. Results: In the presence of mechanical stretch, 100 ng/ml LPS significantly increased IL-8 production after 4 h of 5% stretch (p < 0.05). In the presence of LPS, stretch enhanced LPS-induced IL-8 protein production in a force-, time- and frequency-dependent manner. At both the 1- and 4-hour time points, mechanical stretch and LPS increased IL-8 mRNA levels, respectively, and stretch enhanced LPS-induced IL-8 mRNA levels (p < 0.05). Conclusions: Using cytomechanic methods, we found a synergistic effect of LPS and mechanical stretch on IL-8 production. The response of alveolar type II cells to mechanical stretch depends on their different pathologic states and the applied mechanical stretch, which may reversely influence the outcome of patients with acute respiratory distress syndrome.

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Epidemiology and outcome of acute lung injury in European intensive care units

Cited by 552 publications

References 41 publications

Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome

Diagnostic and prognostic values of Club cell protein 16 (CC16) in critical care patients with acute respiratory distress syndrome

Macrophage A2A Adenosinergic Receptor Modulates Oxygen-Induced Augmentation of Murine Lung Injury

Response of Alveolar Type II Epithelial Cells to Mechanical Stretch and Lipopolysaccharide

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