Lung
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Multicenter Study Observational Study
Longitudinal lung volume changes in patients with chronic obstructive pulmonary disease.
The progression of lung hyperinflation in patients with chronic obstructive pulmonary disease (COPD) has not been studied in a long-term prospective cohort. We explored the longitudinal changes in lung volume compartments with the aim of identifying predictors of a rapid decline of the inspiratory capacity to total lung capacity ratio (IC/TLC). ⋯ MMRC dyspnea scale, post-bronchodilator FEV1, and the Charlson comorbidity index at baseline were independent predictors of a rapid decline in IC/TLC.
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Comparative Study
Angiotensinogen promoter polymorphisms predict low diffusing capacity in U.S. and Spanish IPF cohorts.
Single nucleotide polymorphisms (SNPs) in angiotensinogen (AGT) at positions -20 and -6 are associated with increased severity and progression of various fibrotic diseases. Our earlier work demonstrated that the progression of idiopathic pulmonary fibrosis (IPF) was associated with the A-6 allele. This study examined the hypothesis that the homozygous CC genotype at -20 and the AA genotype at -6 would confer worse measures of pulmonary function (measured by pulmonary function tests) in IPF. ⋯ This study is the first to demonstrate an association of AGT polymorphisms (-20A > C and -6G > A) with lower measures of pulmonary function in IPF. It is also the first to relate the effect of gender in lung fibrosis with polymorphisms in AGT.
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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive dyspnea and worsening lung function. ACE is increased in the bronchoalveolar lavage fluid from patients with IPF, suggesting the role of ACE in the pathogenesis of IPF. We evaluated the role of single-nucleotide polymorphisms (SNPs) in the development risk of IPF. ⋯ This study showed a newly discovered SNP of ACE associated with the risk of development of IPF. ACE -5538T>C and -5508A>C significantly associated with risk of IPF in Korea.
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We investigated rates and predictors of ventilatory support during hospitalization in seemingly not severely compromised nonsurvivors of community-acquired pneumonia (CAP). ⋯ The number of nonsurvivors without obvious reasons for withholding ventilatory support is disturbingly high, particularly in younger patients. Both performance predictors for not being ventilated remain ambiguous, because they may reflect either treatment restrictions or deficient clinical performance. Elucidating this ambiguity will be part of the forthcoming update of the quality assurance program.
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Angiotensin-converting enzyme 2 (ACE2), an ACE homolog, hydrolyzes angiotensin II and opposes its actions, and plays a protective role in the pathogenesis of pulmonary arterial hypertension (PAH). However, the underlying mechanisms involved in the effect of ACE2 on PAH are still uncertain. In this study, we observed the effects of ACE2 activation on endothelial dysfunction and vascular remodeling in the development of severe PAH in rats. ⋯ These findings suggested that ACE2 activation by resorcinolnaphthalein improved endothelial function and suppressed neointimal formation in the prevention of severe PAH by the mechanism of mediating the levels of the components of the renin-angiotensin system.