American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Sep 2023
Meta AnalysisPrevalence, Risk Factors, and Outcomes of Adult Interstitial Lung Abnormalities: A Systematic Review and Meta-Analysis.
Rationale: Incidental parenchymal abnormalities detected on chest computed tomography scans are termed interstitial lung abnormalities (ILAs). ILAs may represent early interstitial lung disease (ILD) and are associated with an increased risk of progressive fibrosis and mortality. The prevalence of ILAs is unknown, with heterogeneity across study populations. ⋯ Older age, male sex, and lower FVC% were associated with greater odds of ILA. Conclusions: Populations undergoing imaging for non-ILD indications demonstrate high ILA prevalence. Standardized reporting and follow-up of ILAs is needed, including defining those at greatest risk of progression to ILD.
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Am. J. Respir. Crit. Care Med. · Sep 2023
Deep Learning Assessment of Progression of Emphysema and Fibrotic Interstitial Lung Abnormality.
Rationale: Although studies have evaluated emphysema and fibrotic interstitial lung abnormality individually, less is known about their combined progression. Objectives: To define clinically meaningful progression of fibrotic interstitial lung abnormality in smokers without interstitial lung disease and evaluate the effects of fibrosis and emphysema progression on mortality. Methods: Emphysema and pulmonary fibrosis were assessed on the basis of baseline and 5-year follow-up computed tomography scans of 4,450 smokers in the COPDGene Study using deep learning algorithms. ⋯ On the basis of this threshold, 2,822 (63%) had progression of neither emphysema nor fibrosis, 841 (19%) had emphysema progression alone, 512 (12%) had fibrosis progression alone, and 275 (6.2%) had progression of both. Compared with nonprogressors, hazard ratios for mortality were 1.42 (95% confidence interval, 1.11-1.82) in emphysema progressors, 1.49 (1.14-1.94) in fibrosis progressors, and 2.18 (1.58-3.02) in those with progression of both emphysema and fibrosis. Conclusions: In smokers without known interstitial lung disease, small changes in fibrosis may be clinically significant, and combined progression of emphysema and fibrosis is associated with increased mortality.
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Am. J. Respir. Crit. Care Med. · Sep 2023
Multicenter StudyMortality in Patients with Obesity and ARDS Receiving ECMO: The Multicenter ECMObesity Study.
Rationale: Patients with obesity are at increased risk for developing acute respiratory distress syndrome (ARDS). Some centers consider obesity a relative contraindication to receiving extracorporeal membrane oxygenation (ECMO) support, despite growing implementation of ECMO for ARDS in the general population. Objectives: To investigate the association between obesity and mortality in patients with ARDS receiving ECMO. ⋯ In propensity score matching of 199 patients with obesity to 199 patients without, patients with obesity had a lower probability of ICU death than those without (22.6% vs. 35.2%; P = 0.007). Conclusions: Among patients receiving ECMO for ARDS, those with obesity had lower ICU mortality than patients without obesity in multivariable and propensity score matching analyses. Our findings support the notion that obesity should not be considered a general contraindication to ECMO.
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Am. J. Respir. Crit. Care Med. · Sep 2023
Single Cell Multiomics Identifies Cells and Genetic Networks Underlying Alveolar Capillary Dysplasia.
Rationale: Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a lethal developmental disorder of lung morphogenesis caused by insufficiency of FOXF1 (forkhead box F1) transcription factor function. The cellular and transcriptional mechanisms by which FOXF1 deficiency disrupts human lung formation are unknown. Objectives: To identify cell types, gene networks, and cell-cell interactions underlying the pathogenesis of ACDMPV. ⋯ Pathogenic variants involving the FOXF1 gene locus disrupt gene expression in EC progenitors, inhibiting the differentiation or survival of capillary 2 ECs and cell-cell interactions necessary for both pulmonary vasculogenesis and alveolar type 1 cell differentiation. Loss of the pulmonary microvasculature was associated with increased VEGFA (vascular endothelial growth factor A) signaling and marked expansion of systemic bronchial ECs expressing COL15A1 (collagen type XV α 1 chain). Conclusions: Distinct FOXF1 gene regulatory networks were identified in subsets of pulmonary endothelial and fibroblast progenitors, providing both cellular and molecular targets for the development of therapies for ACDMPV and other diffuse lung diseases of infancy.