American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyQuality-adjusted survival in the first year after the acute respiratory distress syndrome.
There is little information on long-term outcome after acute respiratory distress syndrome (ARDS). We measured quality-adjusted survival in the first year after ARDS in a prospective cohort (n = 200). All patients met traditional criteria for ARDS. ⋯ QWB was low at 6 and 12 mo (0.59 +/- 0.015 and 0.60 +/- 0.015), yielding a quality-adjusted survival of 36 QALYs per 100 patients (sensitivity range: 21 to 46 QALYs). We conclude that ARDS developing in previously healthy patients is associated with poor quality-adjusted survival. These data are important for cost-effectiveness analyses and long-term care.
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Am. J. Respir. Crit. Care Med. · May 2001
Inspiratory capacity, dynamic hyperinflation, breathlessness, and exercise performance during the 6-minute-walk test in chronic obstructive pulmonary disease.
Patients with severe chronic obstructive pulmonary disease (COPD) develop dynamic lung hyperinflation (DH) during symptom-limited incremental and constant work exercise with cycle ergometer and treadmill. The increase in end-expiratory lung volume seems to be the best predictor of dyspnea. Quantification of DH is based on the relatively complex use of on-line measurement of inspiratory capacity (IC) from flow volume loops. ⋯ Exertional dyspnea correlated with DeltaIC (r = -0.49, p < 0.00001) and baseline MRC (r = 0.59, p < 0.00001). In many patients with COPD, walking leads to DH that can be easily determined with simple spirometric testing. DH helps explain exercise capacity limitation and breathlessness during simple daily activities.
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyComputed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome.
Computed tomography (CT) assessment of positive end-expiratory pressure (PEEP)-induced alveolar recruitment is classically achieved by quantifying the decrease in nonaerated lung parenchyma on a single juxtadiaphragmatic section (Gattinoni's method). This approach ignores the alveolar recruitment occurring in poorly aerated lung areas and may not reflect the alveolar recruitment of the entire lung. This study describes a new CT method in which PEEP-induced alveolar recruitment is computed as the volume of gas penetrating in poorly and nonaerated lung regions following PEEP. ⋯ PEEP-induced alveolar recruitment was 499 +/- 279 ml whereas distension and overdistension of previously aerated lung areas were 395 +/- 382 ml and 28 +/- 6 ml, respectively. The alveolar recruitment according to Gattinoni's method was 26 +/- 24 g and no correlation was found between both methods. A significant correlation was found between PEEP-induced alveolar recruitment and increase in Pa(O(2)) only when recruitment was assessed by the new method (Rho = 0.76, p = 0.003), suggesting that it may be more accurate than Gattinoni's method.
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyPulmonary edema fluid from patients with acute lung injury augments in vitro alveolar epithelial repair by an IL-1beta-dependent mechanism.
Efficient alveolar epithelial repair is crucial for the restoration of the injured alveolar epithelial barrier in patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). We hypothesized that pulmonary edema fluid from patients with ALI /ARDS would inhibit alveolar epithelial repair as measured in an in vitro epithelial wound-repair model using the human alveolar epithelial-like cell line A549. In contrast to our initial hypothesis, pulmonary edema fluid from patients with ALI/ARDS increased alveolar epithelial repair by 33 +/- 3% compared with pooled plasma from healthy donors (p < 0.01). ⋯ Inhibition of interleukin-1beta (IL-1beta) activity by IL-1 receptor antagonist reduced alveolar epithelial repair induced by ALI/ARDS edema fluid by 46 +/- 4% (p < 0.001), indicating that IL-1beta contributed significantly to the increased epithelial repair. In summary, pulmonary edema fluid collected early in the course of ALI/ARDS increased alveolar epithelial repair in vitro by an IL-1beta-dependent mechanism. These data demonstrate a novel role for IL-1beta in patients with ALI/ARDS, indicating that IL-1beta may promote repair of the injured alveolar epithelium.
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Am. J. Respir. Crit. Care Med. · May 2001
Comparative StudyIncreased expression of transforming growth factor-beta1 in small airway epithelium from tobacco smokers and patients with chronic obstructive pulmonary disease (COPD).
Tobacco smoke is believed to cause small airway disease and then chronic obstructive pulmonary disease (COPD), but the molecular mechanisms by which small airway obstruction occurs remain unknown. To study the gene expression levels of transforming growth factor (TGF)-beta1, a potent fibrogenic factor, in small airway epithelium from smokers and patients with COPD, we harvested highly pure samples of epithelial cells from small airways under direct vision by using an ultrathin bronchofiberscope BF-2.7T (outer diameter 2.7 mm with a biopsy channel of 0.8 mm in diameter). The expression levels of TGF-beta1 were evaluated by reverse transcription-polymerase chain reaction (RT-PCR). ⋯ Spontaneously released immunoreactive TGF-beta1 levels from cultured epithelial cells were more elevated in subjects with a history of smoking and patients with COPD than in nonsmokers. Our study showed a close link between smoking and expression of TGF-beta1 in small airways. Our results also suggested that small airway epithelial cells might be involved in obstructive changes found in smokers and patients with COPD.