scholarly journals Biomarker profiles of coagulopathy and alveolar epithelial injury in acute respiratory distress syndrome with idiopathic/immune-related disease or common direct risk factors

Critical Care ◽  
2019 ◽  
Vol 23 (1) ◽  
Author(s):  
Kansuke Koyama ◽  
Shinshu Katayama ◽  
Ken Tonai ◽  
Jun Shima ◽  
Toshitaka Koinuma ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Related Disease ◽  
Alveolar Epithelial Injury

scholarly journals Distinct Time Courses and Pathogenic Contributions of Alveolar Epithelial and Endothelial Injury in Acute Respiratory Distress Syndrome With COVID-19: Evidence From Circulating Biomarkers

2021 ◽  
Author(s):  
Kentaro Tojo ◽  
Natsuhiro Yamamoto ◽  
Takahiro Mihara ◽  
Miyo Abe ◽  
Takahisa Goto
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Tissue Injury ◽  
Endothelial Injury ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Srage Level ◽  
Alveolar Tissue

Abstract Background: In severe cases of coronavirus disease (COVID-19), acute respiratory distress syndrome (ARDS) with alveolar tissue injury occurs. However, the time course and specific contributions of alveolar epithelial and endothelial injury to the pathogenesis of COVID-19 ARDS remain unclear.Methods: We evaluated the levels of a circulating alveolar epithelial injury marker (soluble receptor for advanced glycation end-products: sRAGE) and an endothelial injury marker (angiopoietin-2: ANG-2), along with an alveolar permeability indicator (surfactant protein D: SP-D) in 107 serum samples from nine patients with ARDS and eight without ARDS, all with COVID-19, admitted to Yokohama City University Hospital from January to July 2020. We compared the initial levels of these markers between ARDS and non-ARDS patients, and analysed the temporal changes of these markers in ARDS patients. Results: All the initial levels of sRAGE (median: 2680 pg/mL, IQR:1522–5076 vs. median 701 pg/mL, IQR:344–1148.0, p=0.0152), ANG-2 (median: 699 pg/mL, IQR: 410-2501 vs. median: 231 pg/mL, IQR: 64-584, p=0.0464), and SP-D (median: 17542 pg/mL, IQR: 7423-22979 vs. 1771 pg/mL, IQR: 458-204, p=0.0274) were significantly higher in the ARDS patients than in the non-ARDS patients. The peak sRAGE level in the ARDS patients was observed at the very early phase of disease progression (median: day 1, IQR: day 1–3.5). However, the peaks of ANG-2 (median: day 4, IQR: day 2.5–6) and SPD (median: day 5, IQR: day 3–7.5) were observed at a later phase. Moreover, the ANG-2 level was significantly correlated with the arterial oxygenation (p=0.030) and the SPD level (p=0.002), but the sRAGE level was not. Conclusion: Evaluation of circulating markers confirms that COVID-19 ARDS is characterised by severe alveolar tissue injury. Our data indicate that the endothelial injury, which continues for a longer period than the epithelial injury, seems to be the main contributor to alveolar barrier disruption. Targeting the endothelial injury may, thus, be a promising approach to overcome ARDS with COVID-19.

scholarly journals Distinct time courses and pathogenic contributions of alveolar epithelial and endothelial injury in acute respiratory distress syndrome with COVID-19: evidence from circulating biomarkers

2021 ◽  
Author(s):  
Kentaro Tojo ◽  
Natsuhiro Yamamoto ◽  
Takahiro Mihara ◽  
Miyo Abe ◽  
Takahisa Goto
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Tissue Injury ◽  
Endothelial Injury ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Srage Level ◽  
Alveolar Tissue

AbstractBackgroundIn severe cases of coronavirus disease (COVID-19), acute respiratory distress syndrome (ARDS) with alveolar tissue injury occurs. However, the time course and specific contributions of alveolar epithelial and endothelial injury to the pathogenesis of COVID-19 ARDS remain unclear.MethodsWe evaluated the levels of a circulating alveolar epithelial injury marker (soluble receptor for advanced glycation end-products: sRAGE) and an endothelial injury marker (angiopoietin-2: ANG-2), along with an alveolar permeability indicator (surfactant protein D: SP-D) in 107 serum samples from nine patients with ARDS and eight without ARDS, all with COVID-19. We compared the initial levels of these markers between ARDS and non-ARDS patients, and analysed the temporal changes of these markers in ARDS patients.FindingsAll the initial levels of sRAGE, ANG-2, and SP-D were significantly higher in the ARDS patients than in the non-ARDS patients. The peak sRAGE level in the ARDS patients was observed at the very early phase of disease progression. However, the peaks of ANG-2 and SPD were observed at a later phase. Moreover, the ANG-2 level was significantly correlated with the arterial oxygenation and the SPD level, but the sRAGE level was not.InterpretationEvaluation of circulating markers confirms that COVID-19 ARDS is characterised by severe alveolar tissue injury. Our data indicate that the endothelial injury, which continues for a longer period than the epithelial injury, seems to be the main contributor to alveolar barrier disruption. Targeting the endothelial injury may, thus, be a promising approach to overcome ARDS with COVID-19.FundingNone

Prognostic factors for development of acute respiratory distress syndrome following traumatic injury – a systematic review and meta-analysis

2021 ◽  
pp. 2100857
Author(s):  
Alexandre Tran ◽  
Shannon M. Fernando ◽  
Laurent J. Brochard ◽  
Eddy Fan ◽  
Kenji Inaba ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Respiratory Distress Syndrome ◽  
Prognostic Factors ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Traumatic Injury ◽  
Clinical Risk Factors ◽  
Factors Associated ◽  
Post Traumatic

PurposeTo summarise the prognostic associations between various clinical risk factors and the development of the acute respiratory distress syndrome (ARDS) following traumatic injury.MethodsWe conducted this review in accordance with the PRISMA and CHARMS guidelines. We searched six databases from inception through December 2020. We included English language studies describing the clinical risk factors associated with the development of post-traumatic ARDS, as defined by either the American-European Consensus Conference or the Berlin definition. We pooled adjusted odds ratios for prognostic factors using the random effects method. We assessed risk of bias using the QUIPS tool and certainty of findings using GRADE methodology.ResultsWe included 39 studies involving 5 350 927 patients. We identified the amount of crystalloid resuscitation as a potentially modifiable prognostic factor associated with the development of post-traumatic ARDS (adjusted odds ratio [aOR] 1.19 for each additional liter of crystalloid administered within first 6 h after injury, 95% CI 1.15 to 1.24, high certainty). Non-modifiable prognostic factors with a moderate or high certainty of association with post-traumatic ARDS included increasing age, non-Hispanic white race, blunt mechanism of injury, presence of head injury, pulmonary contusion, or rib fracture; and increasing chest injury severity.ConclusionWe identified one important modifiable factor, the amount of crystalloid resuscitation within the first 24 h of injury, and several non-modifiable factors associated with development of post-traumatic ARDS. This information should support the judicious use of crystalloid resuscitation in trauma patients and may inform the development of a risk-stratification tools.

Acute respiratory distress syndrome in cancer patients: Epidemiology, risk factors, and outcomes

2017 ◽  
Vol 42 ◽  
pp. 390
Author(s):  
Eduardo Mantovani Cardoso ◽  
Aniele Tomadon ◽  
Keli Lovison ◽  
Péricles Almeida Delfino Duarte
Keyword(s):  
Risk Factors ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Cancer Patients ◽  
Distress Syndrome

scholarly journals Acute respiratory distress syndrome mimickers lacking common risk factors of the Berlin definition

2015 ◽  
Vol 42 (2) ◽  
pp. 164-172 ◽  
Author(s):  
Aude Gibelin ◽  
Antoine Parrot ◽  
Bernard Maitre ◽  
Christian Brun-Buisson ◽  
Armand Mekontso Dessap ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Berlin Definition ◽  
Common Risk Factors

scholarly journals Alveolar CCN1 is associated with mechanical stretch and acute respiratory distress syndrome severity

2020 ◽  
Vol 319 (5) ◽  
pp. L825-L832
Author(s):  
Eric D. Morrell ◽  
Serge Grazioli ◽  
Chi Hung ◽  
Osamu Kajikawa ◽  
Susanna Kosamo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Mechanical Stretch ◽  
Mechanically Ventilated ◽  
Alveolar Epithelial ◽  
Protein Levels

The cellular communication network factor 1 (CCN1) is a matricellular protein that can modulate multiple tissue responses, including inflammation and repair. We have previously shown that adenoviral overexpression of Ccn1 is sufficient to cause acute lung injury in mice. We hypothesized that CCN1 is present in the airspaces of lungs during the acute phase of lung injury, and higher concentrations are associated with acute respiratory distress syndrome (ARDS) severity. We tested this hypothesis by measuring 1) CCN1 in bronchoalveolar lavage fluid (BALF) and lung homogenates from mice subjected to ventilation-induced lung injury (VILI), 2) Ccn1 gene expression and protein levels in MLE-12 cells (alveolar epithelial cell line) subjected to mechanical stretch, and 3) CCN1 in BALF from mechanically ventilated humans with and without ARDS. BALF CCN1 concentrations and whole lung CCN1 protein levels were significantly increased in mice with VILI ( n = 6) versus noninjured controls ( n = 6). Ccn1 gene expression and CCN1 protein levels were increased in MLE-12 cells cultured under stretch conditions. Subjects with ARDS ( n = 77) had higher BALF CCN1 levels compared with mechanically ventilated subjects without ARDS ( n = 45) ( P < 0.05). In subjects with ARDS, BALF CCN1 concentrations were associated with higher total protein, sRAGE, and worse [Formula: see text]/[Formula: see text] ratios (all P < 0.05). CCN1 is present in the lungs of mice and humans during the acute inflammatory phase of lung injury, and concentrations are higher in patients with increased markers of severity. Alveolar epithelial cells may be an important source of CCN1 under mechanical stretch conditions.

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